Usefulness of the Agatston score = 0 to exclude ischemic cardiomyopathy in patients with heart failure.

Quantification of coronary artery calcium has prognostic value and is commonly used in asymptomatic patients. Routine clinical use of coronary artery calcium in other populations remains uncertain. We sought to understand the potential application of the Agatston score in patients with heart failure (HF). For this purpose, 3 populations were identified: (1) patients with an Agatston score equal to 0, (2) patients with high-risk coronary artery disease (CAD) defined as 3-vessel, left main, or 2-vessel disease involving the proximal left anterior descending coronary artery, and (3) patients with HF symptoms and left ventricular (LV) ejection fraction <50%. Excluding patients with HF or LV dysfunction, 738 patients (mean age 52 ± 10 years, 43% men) had an Agatston score equal to 0. Of these, 18 (2%) had obstructive CAD (diameter stenosis ≥50%), 8 (1%) had diameter stenoses ≥70%, and none had high-risk CAD. The 74 patients with high-risk CAD without LV dysfunction had high Agatston scores (mean 895 ± 734, median 716, range 50 to 3,210). In total 153 patients with a history of HF and abnormal ejection fraction were identified. All 13 patients with ischemic cardiomyopathy had Agatston scores >0, whereas 46 of 140 patients (30.1%) with nonischemic causes had an Agatston score equal to 0. An Agatston score equal to 0 identified nonischemic causes with a specificity of 100% (confidence interval 90 to 100) and positive predictive value of 100% (confidence interval 90 to 100). Agatston score equal to 0 had incremental value to pretest probability for CAD. In conclusion, an Agatston score equal to 0 confers a very low likelihood of obstructive CAD, appears to rule out high-risk CAD, and thus may be used to rule out ischemic cardiomyopathy in patients with HF.

Quadricuspid Aortic Valve Diagnosed by Cardiac CT.

Quadricuspid aortic valves are rare congenital anomalies which can be diagnosed by various imaging modalities. Described is the case of a 77 year old female with a quadricuspid aortic valve diagnosed by cardiac CT.

Thromboembolism in heart transplantation: role of prothrombin G20210A and factor V Leiden.

BACKGROUND: Thromboembolism has been reported as a frequent complication after cardiac transplantation. Many risk factors for thrombosis may explain this, such as metabolic alterations and the use of cyclosporine. In the general population, two single nucleotide polymorphisms (SNPs), factor V Leiden and prothrombin G20210A (PT G20210A), have been associated with a significant increase in the risk of thrombosis. However, these mutations have not been analyzed in cardiac transplant patients. We describe the protracted history of recurrent thromboembolism in a rare case of homozygosity for the PT G20210A variant. This prompted us to analyze the entire cardiac transplant cohort for the incidence of thromboembolic events and their association with these genetic polymorphisms. METHODS: We report the study of 84 cardiac transplant recipients. We retrospectively analyzed the frequency of thromboembolic episodes. The genotypes for FVL and PT G20210A were determined and correlated with those episodes. RESULTS: Our results confirm a very high incidence of thromboembolism in this population. We also found a significant increase in the likelihood of thromboembolism in subjects with the PTB G20210A variant (odds ratio 3.08; 95% confidence interval: 1.7-5.5). CONCLUSIONS: The incidence of thromboembolic complications after heart transplantation is increased and may be related in part to genetic predisposition.

Genetic polymorphisms predisposing to hyperhomocysteinemia in cardiac transplant patients.

Genetic determinants for high homocysteine (Hcy) levels are now well known. We studied several single nucleotide polymorphisms (SNP) in Hcy-regulating genes [methylenetetrahydrofolate reductase (MTHFR) C677T and A1298C; methionine synthase (MS) A2756G; methionine synthase reductase (MTRR) A66G] in relation to total plasma Hcy levels, transplant coronary artery disease and thromboembolic episodes in 84 heart transplant patients, and we compared the incidence of these polymorphisms with those in a healthy adult controls. At least one copy of the G allele of the MTRR A66G SNP was found in a significantly greater proportion of cardiac transplant (CTX) recipients compared with controls (94.0% vs. 79.9% respectively). None of the SNP analyzed were correlated with total Hcy plasma levels or the presence of transplant coronary artery disease. However, MS A2756G was significantly associated with cobalamin levels (AA genotype: 290 +/- 122 pmol/l; AG: 381 +/- 151 pmol/l and GG: 415 +/- 100 pmol/l), as was MTRR A66G (AA: 478 +/- 219 pmol/l, AG: 306 +/- 124 pmol/l and GG: 306 +/- 123 pmol/l). MTRR A66G was also correlated with serum folate. No association was found with thromboembolic events. In conclusion, there was a significant difference in the frequency of the G allele genotype of the MTRR A66G in CTX patients versus controls. Differences in cobalamin and folate levels with the MTRR A66G and MS A2756G polymorphisms were noted. Thus, SNP in Hcy-regulating genes may be important determinants of vitamin metabolism in CTX, raising the question of increased vitamin requirements to minimize increased plasma Hcy in this high-risk group.