929-63 Dobutamine Stress Cine Magnetic Resonance Imaging versus PET for Detection of Myocardial Viability

To identify viable myocardium before coronary revascularization, we prospectively submitted eleven patients (60±7 yrs; 11 M) with previous Q-wave myocardial infarction to 18FDG-Positon Emission Tomography and low-dose (5 to 10 μg/kg/min) dobutamine cine-MRI. 18FDG uptake > 60% was considered indicative of viable tissue. Ouantitation of systolic wall thickening/thinning (SW) was performed by use of a computer software allowing automatic detection of epicardial and endocardial outlines, at rest and under 5, 7.5 and 10 μg/kg/min of dobutamine. Heart slices of both 18FDG-PET scans and dobutamine cine-MRI were divided in 8 segments, matched and analyzed byobservers blinded to clinical data. Sixty-five segments were considered viable by 18FDG-PET; in this subgroup, rest SW thickening averaged 47±5% and improved by 43±8% under low-dose dobutamine. In the remaining 23 segments considered non viable by PET. rest SW thickening averaged 14±7%*(*p<0.05 vs viable segment group) and further worsened by –13±8%*during low-dose dobutamine stress (*p<0.05 versus viable segment group). Positive predictive value of low-dose dobutamine stress cine-MRI for assessment of myocardial viability was 84%. These data suggest that quantitative assessment of regional wall motion by dobutamine cine-MRI may help discriminate viable from non viable myocardium as defined by 18FDG-Positon Emission Tomography

Preventing acute decrease in renal function induced by coronary angiography (PRECORD): a prospective randomized trial

SummaryBackgroundInfusion of saline attenuates the decrease in renal function induced by radiographic contrast agents among patients with chronic renal insufficiency.AimThe Preventing Renal alteration in Coronary Disease (PRECORD) trial was a randomized trial to assess the effect on renal function of saline infusion during and after coronary angiography in 201 patients without severe chronic renal insufficiency (serum creatinine<140μmol/L).MethodsAll patients received standard oral hydration: 2000mL of tap water within the 24hours after coronary angiography. Patients were randomized before the procedure to intravenous hydration (1000mL of 0.9% saline infusion) or no additional hydration. The infusion was started in the catheterization laboratory and continued for 24hours. The primary endpoint was the change in calculated creatinine clearance between baseline and 24hours after coronary angiography. The same ionic low osmolar radiographic contrast agent (ioxaglate) was used in all patients.ResultsBoth groups had similar baseline characteristics, including age, serum creatinine, volume of contrast and proportion of patients undergoing ad hoc coronary angioplasty. The overall decrease in serum creatinine clearance 24hours after the procedure was –3.44 (0.68)mL/min. The change in serum creatinine clearance 24hours after the procedure was –2.81 (1.07)mL/min in the infusion group vs –4.09 (0.91)mL/min in the control group (p=0.38).ConclusionRenal function is altered only slightly 24hours after coronary angiography with standard oral hydration alone and is not affected by saline infusion started at the beginning of coronary angiography, even in patients with mild-to-moderate renal dysfunction

Effect of Cyclosporine on Left Ventricular Remodeling After Reperfused Myocardial Infarction

ObjectivesThis study examined the effect of a single dose of cyclosporine administered at the time of reperfusion on left ventricular (LV) remodeling and function by cardiac magnetic resonance 5 days and 6 months after myocardial infarction.BackgroundIn a human study, administration of cyclosporine at the time of acute reperfusion was associated with a smaller infarct size.MethodsTwenty-eight patients of the original cyclosporine study had an acute (at 5 days) and a follow-up (at 6 months) cardiac magnetic resonance study to determine LV volumes, mass, ejection fraction, myocardial wall thickness in infarcted and remote noninfarcted myocardium, and infarct size.ResultsThere was a persistent reduction in infarct size at 6 months in the cyclosporine group compared with the control group of patients (29 ± 15 g vs. 38 ± 14 g; p = 0.04). There was a significant reduction of LV end-systolic volume (and a trend for LV end-diastolic volume; p = 0.07) in the cyclosporine group compared with the control group, both at 5 days and 6 months after infarction. There was no significant difference between the 2 groups in either global LV mass or regional wall thickness of the remote noninfarcted myocardium at 5 days or 6 months. Attenuation of LV dilation and improvement of LV ejection fraction by cyclosporine at 6 months were correlated with infarct size reduction.ConclusionsCyclosporine used at the moment of acute myocardial infarction reperfusion persistently reduces infarct size and does not have a detrimental effect on LV remodeling. These results are preliminary and must be supported by further studies. (Ciclosporin A and Acute Myocardial Infarction; NCT00403728

A human MYBPC3 mutation appearing about 10 centuries ago results in a hypertrophic cardiomyopathy with delayed onset, moderate evolution but with a risk of sudden death.

BACKGROUND: Hypertrophic Cardiomyopathy (HCM) is a genetically heterogeneous disease. One specific mutation in the MYBPC3 gene is highly prevalent in center east of France giving an opportunity to define the clinical profile of this specific mutation. METHODS: HCM probands were screened for mutation in the MYH7, MYBPC3, TNNT2 and TNNI3 genes. Carriers of the MYBPC3 IVS20-2A&gt;G mutation were genotyped with 8 microsatellites flanking this gene. The age of this MYBPC3 mutation was inferred with the software ESTIAGE. The age at first symptom, diagnosis, first complication, first severe complication and the rate of sudden death were compared between carriers of the IVS20-2 mutation (group A) and carriers of all other mutations (group B) using time to event curves and log rank test. RESULTS: Out of 107 HCM probands, 45 had a single heterozygous mutation in one of the 4 tested sarcomeric genes including 9 patients with the MYBPC3 IVS20-2A&gt;G mutation. The IVS20-2 mutation in these 9 patients and their 25 mutation carrier relatives was embedded in a common haplotype defined after genotyping 4 polymorphic markers on each side of the MYBPC3 gene. This result supports the hypothesis of a common ancestor. Furthermore, we evaluated that the mutation occurred about 47 generations ago, approximately at the 10th century.We then compared the clinical profile of the IVS20-2 mutation carriers (group A) and the carriers of all other mutations (group B). Age at onset of symptoms was similar in the 34 group A cases and the 73 group B cases but group A cases were diagnosed on average 15 years later (log rank test p = 0.022). Age of first complication and first severe complication was delayed in group A vs group B cases but the prevalence of sudden death and age at death was similar in both groups. CONCLUSION: A founder mutation arising at about the 10th century in the MYBPC3 gene accounts for 8.4% of all HCM in center east France and results in a cardiomyopathy starting late and evolving slowly but with an apparent risk of sudden death similar to other sarcomeric mutations