14 research outputs found
The prognostic value of left ventricular mechanical dyssynchrony using gated myocardial perfusion imaging in patients with end-stage renal disease
No full textBackground. Prior studies show that left ventricular mechanical dyssynchrony (LVD), measured by gated SPECT myocardial perfusion imaging (MPI), identifies patients with end-stage renal disease (ESRD) at higher risk for all-cause mortality but these were in small number of patients. We sought to assess the interaction between LVD and LV perfusion pattern in risk-stratification of a large sample size of patients with ESRD. Methods. From the renal transplantation database maintained at the University of Alabama at Birmingham, we identified consecutive patients with ESRD who had gated SPECT MPI between 2003 and 2007. MPIs were reprocessed to derive LV ejection fraction (EF), perfusion defect size, and LVD [phase bandwidth (BW) and phase standard deviation (SD)]. The primary end-point was all-cause mortality, which was prospectively collected and verified against the social security death index database. Results. There were 828 patients aged 52.6 ± 0.36 years (45percent were women and 60percent had diabetes mellitus). The LVEF was 54.8 ± 0.4percent and the perfusion pattern was abnormal in 334 patients (41percent). During a follow-up period of 61 ± 0.9 months, 230 patients (28percent) received renal transplants and 290 patients (35percent) died. The phase BW (73.1 ± 2.6°vs 66.3 ± 1.8°, P = .02) and SD (25.2 ± 0.8°vs 23.4 ± 0.5°, P = .06) were greater in patients who died than those who survived indicating greater dyssynchrony. Patients with phase BW 56°or SD ≥21°(median values) had worse 5-year survival (64percent vs 72percent, and 66percent vs 71percent, log-rank P = .005 and P = .07, respectively). After adjusting for demographics, co-morbidities, LVEF, and perfusion pattern, phase BW was associated with worse outcome (hazard ratio 1.289 95percent CI 1.010-1.644, P = .04). Conclusions. LVD by phase analysis of gated SPECT MPI provides prognostic value in ESRD beyond myocardial perfusion and EF. © 2014 American Society of Nuclear Cardiology.AlJaroudi W, 2011, J NUCL CARDIOL, V18, P36, DOI 10.1007-s12350-010-9296-1; AlJaroudi W, 2010, J NUCL CARDIOL, V17, P1058, DOI 10.1007-s12350-010-9271-x; AlJaroudi W, 2010, AM J CARDIOL, V106, P1042, DOI 10.1016-j.amjcard.2010.05.039; AlJaroudi W, 2012, EUR J NUCL MED MOL I, V39, P1581, DOI 10.1007-s00259-012-2171-3; Al-Jaroudi W, 2011, AM J CARDIOL, V107, P1235, DOI 10.1016-j.amjcard.2010.12.024; AlJaroudi WA, 2010, J NUCL CARDIOL, V17, P398, DOI 10.1007-s12350-009-9169-7; Chen J, 2011, J NUCL CARDIOL, V18, P299, DOI 10.1007-s12350-010-9331-2; Chen J, 2005, J NUCL CARDIOL, V12, P687, DOI 10.1016-j.nuclcard.2005.06.088; Delgado V, 2011, CIRCULATION, V123, P70, DOI 10.1161-CIRCULATIONAHA.110.945345; GERMANO G, 1995, J NUCL MED, V36, P2138; Hage FG, 2007, AM J CARDIOL, V100, P1020, DOI 10.1016-j.amjcard.2007.04.045; Hage FG, 2009, J AM COLL CARDIOL, V53, P2129, DOI 10.1016-j.jacc.2009.02.047; Hage FG, 2011, J NUCL CARDIOL, V18, P1086, DOI 10.1007-s12350-011-9429-1; Hage FG, 2010, J NUCL CARDIOL, V17, P378, DOI 10.1007-s12350-010-9199-1; Hellman RN, 2011, SEMIN NEPHROL, V31, P310, DOI 10.1016-j.semnephrol.2011.05.010; Holly TA, 2010, J NUCL CARDIOL, V17, P941, DOI 10.1007-s12350-010-9246-y; Iskandrian AE, 2010, J AM COLL CARDIOL, V55, P231, DOI 10.1016-j.jacc.2009.10.007; Kumar V, 2013, AM J CARDIOL, V111, P291, DOI 10.1016-j.amjcard.2012.09.029; Murata T, 2011, NEPHROL DIAL TRANSPL, V26, P1655, DOI 10.1093-ndt-gfq590; Pazhenkottil AP, 2010, HEART, V97, P33; Shlipak MG, 2013, NEW ENGL J MED, V369, P932, DOI 10.1056-NEJMoa1214234; United States Renal Data System (USRDS), 2012 ANN DAT REP ATL; Venkataraman R, 2008, AM J CARDIOL, V102, P1451, DOI 10.1016-j.amjcard.2008.07.02912
Comparison of three commercially available softwares for measuring left ventricular perfusion and function by gated SPECT myocardial perfusion imaging
No full textBackground. The three softwares, Quantitative Perfusion SPECT (QPS), Emory Cardiac Toolbox, and 4 Dimension-Myocardial SPECT (4DM) are widely used with myocardial perfusion imaging (MPI) to determine perfusion defect size (PDS) and left ventricular (LV) function. There are limited data on the degree of agreement between these methods in quantifying the LV perfusion pattern and function. Methods and Results. In 120 consecutive patients who had abnormal regadenoson SPECT MPI with a visually derived summed stress score ≥4, the correlation between the softwares for measurements of PDS, reversible, and fixed defects was poor to fair (Spearman's ρ = 0.18-0.72). Overall, estimation of defect size was smaller by QPS and larger by 4DM. There was discordance among the softwares in 62percent of the cases in defining PDS as small-moderate-large. The correlation between the softwares was better for measuring LVEF, volumes and mass (ρ = 0.84-0.97), and discrepant results for defining normal-mild-moderate-severe LV systolic dysfunction were prevalent in 28percent of the patients. Conclusion. There are significant differences between the softwares in measuring PDS as well as LV function, and more importantly in defining small, moderate, or large ischemic burden. These results suggest the necessity of using the same software when assessing interval changes by serial imaging. © 2014 American Society of Nuclear Cardiology.Akesson L, 2004, CLIN PHYSIOL FUNCT I, V24, P374, DOI 10.1111-j.1475-097X.2004.00574.x; Schocken DD, 2008, CIRCULATION, V117, P2544, DOI 10.1161-CIRCULATIONAHA.107.188965; [Anonymous], 2013, INT STUDY COMP HLTH; Bax JJ, 2000, AM J CARDIOL, V86, P1299, DOI 10.1016-S0002-9149(00)01231-5; Chrysanthou-Baustert I, 2013, J NUCL CARDIOL, V20, P609, DOI 10.1007-s12350-013-9726-y; FABER TL, 1995, J NUCL MED, V36, P697; Ficaro EP, 2007, J NUCL CARDIOL, V14, P455, DOI 10.1016-j.nuclcard.2007.06.006; Garcia EV, 2007, J NUCL CARDIOL, V14, P420, DOI 10.1016-j.nuclcard.2007.06.009; GERMANO G, 1995, J NUCL MED, V36, P2138; Germano G, 2007, J NUCL CARDIOL, V14, P433, DOI 10.1016-j.nuclcard.2007.06.008; Guner LA, 2010, EUR J NUCL MED MOL I, V37, P2070, DOI 10.1007-s00259-010-1522-1; Hachamovitch R, 2003, CIRCULATION, V107, P2900, DOI 10.1161-01.CIR.0000072790.23090.41; Hachamovitch R, 2002, CIRCULATION, V105, P823, DOI 10.1161-hc0702.103973; Hage FG, 2012, J NUCL CARDIOL, V19, P1102, DOI 10.1007-s12350-012-9625-7; Hedeer Fredrik, 2010, BMC Med Imaging, V10, P10, DOI 10.1186-1471-2342-10-10; Holly TA, 2010, J NUCL CARDIOL, V17, P941, DOI 10.1007-s12350-010-9246-y; Iskandrian AE, 2014, JACC-CARDIOVASC IMAG, V7, P79, DOI 10.1016-j.jcmg.2013.05.022; Jessup M, 2009, CIRCULATION, V119, P1977, DOI 10.1161-CIRCULATIONAHA.109.192064; Kakhki VRD, 2007, HELL J NUCL MED, V10, P19; Khalil MM, 2006, NUCL MED COMMUN, V27, P321, DOI 10.1097-01.mnm.0000202861.67293.95; Knollmann D, 2008, EUR J NUCL MED MOL I, V35, P311, DOI 10.1007-s00259-007-0600-5; Lima RSL, 2003, J AM COLL CARDIOL, V42, P64, DOI 10.1016-S0735-1097(03)00562-X; Lin G Sharat, 2006, J Nucl Med Technol, V34, P3; LIN LI, 1989, BIOMETRICS, V45, P255, DOI 10.2307-2532051; Lum DP, 2003, NUCL MED COMMUN, V24, P259, DOI 10.1097-01.mnm.0000061047.24401.b6; Nakajima K, 2001, J NUCL MED, V42, P1571; Nichols K, 2000, J NUCL MED, V41, P1308; Schaefer WM, 2005, J NUCL MED, V46, P1256; Shaw LJ, 2012, J NUCL CARDIOL, V19, P1026, DOI 10.1007-s12350-012-9593-y; Slomka PJ, 2006, J NUCL CARDIOL, V13, P642, DOI 10.1016-j.nuclcard.2006.06.131; Svensson A, 2004, EUR J NUCL MED MOL I, V31, P229, DOI 10.1007-s00259-003-1361-4; Wolak A, 2008, J NUCL CARDIOL, V15, P27, DOI 10.1016-j.nuclcard.2007.09.02012
The effect of bone marrow mononuclear stem cell therapy on left ventricular function and myocardial perfusion
No full textBackground: Bone morrow stem cell (BMC) transfer is an emerging therapy with potential to salvage cardiomyocytes during acute myocardial infarction and promote regeneration and endogenous repair of damaged myocardium in patients with left ventricular (LV) dysfunction. We performed a meta-analysis to examine the association between administration of BMC and LV functional recovery as assessed by imaging. Methods and Results: Our meta-analysis included data from 32 trials comprising information on 1,300 patients in the treatment arm and 1,006 patients in the control arm. Overall, BMC therapy was associated with a significant increase in LV ejection fraction by 4.6percent ± 0.7percent (P .001) (control-adjusted increase of 2.8percent ± 0.9percent, P =.001), and a significant decrease in perfusion defect size by 9.5percent ± 1.4percent (P .001) (control-adjusted decrease of 3.8percent ± 1.2percent, P =.002). The effect of BMC therapy was similar whether the cells were administered via intra-coronary or intra-myocardial routes and was not influenced by baseline ejection fraction or perfusion defect size. Conclusions: BMC transfer appears to have a positive impact on LV recovery in patients with acute coronary syndrome and those with stable coronary disease with or without heart failure. Most studies were small and a minority used a core laboratory for image analysis. © 2013 American Society of Nuclear Cardiology.Abdel-Latif A, 2007, ARCH INTERN MED, V167, P989, DOI 10.1001-archinte.167.10.989; Gnecchi M, 2008, CIRC RES, V103, P1204, DOI 10.1161-CIRCRESAHA.108.176826; Assmus B, 2010, CIRC-HEART FAIL, V3, P89, DOI 10.1161-CIRCHEARTFAILURE.108.843243; Assmus B, 2006, NEW ENGL J MED, V355, P1222, DOI 10.1056-NEJMoa051779; Barbash IM, 2003, CIRCULATION, V108, P863, DOI 10.1161-01.CIR.0000084828.50310.6A; Beeres SL, 2006, AM HEART J, V152, P684; Beeres SLMA, 2008, J MAGN RESON IMAGING, V27, P992, DOI 10.1002-jmri.21081; Beeres SLMA, 2006, AM J CARDIOL, V97, P1326, DOI 10.1016-j.amjcard.2005.11.068; Beeres SLMA, 2007, AM J CARDIOL, V100, P1094, DOI 10.1016-j.amjcard.2007.04.056; Beeres SLMA, 2006, J NUCL MED, V47, P574; Beitnes JO, 2009, HEART, V95, P1983, DOI 10.1136-hrt.2009.178913; Bozdag-Turan Ilkay, 2012, BMC Res Notes, V5, P195, DOI 10.1186-1756-0500-5-195; Cao F, 2009, EUR HEART J, V30, P1986, DOI 10.1093-eurheartj-ehp220; Chen Shaoliang, 2006, J Invasive Cardiol, V18, P552; Chen SL, 2004, AM J CARDIOL, V94, P92, DOI 10.1016-j.amjcard.2004.03.034; Dawn B, 2009, ANTIOXID REDOX SIGN, V11, P1865, DOI 10.1089-ARS.2009.2462; Dill T, 2009, AM HEART J, V157, P541, DOI 10.1016-j.ahj.2008.11.011; Egger M, 1997, BRIT MED J, V315, P629; Fazel S, 2006, J CLIN INVEST, V116, P1865, DOI 10.1172-JCI27019; Fu MQ, 2012, INT J CARDIOL, V155, P33, DOI 10.1016-j.ijcard.2011.01.081; Fuchs S, 2006, AM J CARDIOL, V97, P823, DOI 10.1016-j.amjcard.2005.09.132; Giannotti G, 2010, HYPERTENSION, V55, P1389, DOI 10.1161-HYPERTENSIONAHA.109.141614; Grajek S, 2010, EUR HEART J, V31, P691, DOI 10.1093-eurheartj-ehp536; Gruh I, 2006, CIRCULATION, V113, P1326, DOI 10.1161-CIRCULATIONAHA.105.559005; Herbots L, 2009, EUR HEART J, V30, P662, DOI 10.1093-eurheartj-ehn532; Higgins JPT, 2009, COCHRANE HDB SYSTEMA; Higgins JPT, 2002, STAT MED, V21, P1539, DOI 10.1002-sim.1186; Hirsch A, 2011, EUR HEART J, V32, P1736, DOI 10.1093-eurheartj-ehq449; Hopp E, 2011, J CARDIOVASC MAGN R, V13, DOI 10.1186-1532-429X-13-22; Hu SS, 2011, J AM COLL CARDIOL, V57, P2409, DOI 10.1016-j.jacc.2011.01.037; Huikuri HV, 2008, EUR HEART J, V29, P2723, DOI 10.1093-eurheartj-ehn436; Iqbal FM, 2013, J AM COLL CARDIOL; Iskandrian AE, J AM COLL C IN PRESS; Jackson KA, 2001, J CLIN INVEST, V107, P1395, DOI 10.1172-JCI12150; Janssens S, 2006, LANCET, V367, P113, DOI 10.1016-S0140-6736(05)67861-0; Kaminek M, 2008, J NUCL CARDIOL, V15, P392, DOI 10.1016-j.nuclcard.2008.02.016; Kandala J, 2013, AM J CARDIOL, V112, P217, DOI 10.1016-j.amjcard.2013.03.021; Kocher AA, 2001, NAT MED, V7, P430, DOI 10.1038-86498; Kuswardhani R A Tuty, 2011, Acta Med Indones, V43, P168; Landmesser U, 2004, CIRCULATION, V110, P1933, DOI 10.1161-01.CIR.0000143232.67642.7A; Li ZQ, 2007, INT J CARDIOL, V115, P52, DOI 10.1016-j.ijcard.2006.04.005; Lipiec P, 2009, EUR J NUCL MED MOL I, V36, P587, DOI 10.1007-s00259-008-0988-6; Lunde K., 2007, AM HEART J, V154, P710; Lunde K, 2006, NEW ENGL J MED, V355, P1199, DOI 10.1056-NEJMoa055706; Martin-Rendon E, 2008, EUR HEART J, V29, P1807, DOI 10.1093-eurheartj-ehn220; Meluzin J, 2008, INT J CARDIOL, V128, P185, DOI 10.1016-j.ijcard.2007.04.098; Meluzin J, 2006, AM HEART J, V152, P975, DOI DOI 10.1016-S0735-1097(03)00783-6; Meyer GP, 2006, CIRCULATION, V113, P1287, DOI 10.1161-CIRCULATIONAHA.105.575118; Meyer GP, 2009, EUR HEART J, V30, P2978, DOI 10.1093-eurheartj-ehp374; Moher D, 2009, PLOS MED, V21, P6, DOI DOI 10.1371-J0URNAL.PMED.1000097; Murry CE, 2004, NATURE, V428, P664, DOI 10.1038-nature02446; Nygren JM, 2004, NAT MED, V10, P494, DOI 10.1038-nm1040; Orlic D, 2003, PEDIATR TRANSPLANT, V7, P86, DOI 10.1034-j.1399-3046.7.s3.13.x; Pannitteri G, 2006, J CARDIOVASC MED, V7, P872; Perin EC, 2012, JAMA-J AM MED ASSOC, V307, P1717, DOI 10.1001-jama.2012.418; Perin EC, 2011, AM HEART J, V161, P1078, DOI 10.1016-j.ahj.2011.01.028; Roncalli J, 2011, EUR HEART J, V32, P1748, DOI 10.1093-eurheartj-ehq455; Rota M, 2007, P NATL ACAD SCI USA, V104, P17783, DOI 10.1073-pnas.0706406104; Schachinger V, 2006, NEW ENGL J MED, V355, P1210, DOI 10.1056-NEJMoa060186; Shah AM, 2012, JACC-CARDIOVASC IMAG, V5, P1139, DOI 10.1016-j.jcmg.2012.02.019; Sherwood M, 2012, J NUCL CARDIOL, V19, P891, DOI 10.1007-s12350-012-9583-0; Sieveking DP, 2008, J AM COLL CARDIOL, V51, P660, DOI 10.1016-j.jacc.2007.09.059; Sorrentino SA, 2007, CIRCULATION, V116, P163, DOI 10.1161-CIRCULATIONAHA.106.684381; Strauer BE, 2010, EUR J HEART FAIL, V12, P721, DOI 10.1093-eurjhf-hfq095; Templin C, 2011, INT J DEV BIOL, V55, P407, DOI 10.1387-ijdb.103219ct; Tendera M, 2009, EUR HEART J, V30, P1313, DOI 10.1093-eurheartj-ehp073; Traverse JH, 2010, AM HEART J, V160, P428, DOI 10.1016-j.ahj.2010.06.009; Traverse JH, 2011, JAMA-J AM MED ASSOC, V306, P2110, DOI 10.1001-jama.2011.1670; van Ramshorst J, 2009, JAMA-J AM MED ASSOC, V301, P1997, DOI 10.1001-jama.2009.685; Venkataraman R, 2009, JACC-CARDIOVASC IMAG, V2, P1301, DOI 10.1016-j.jcmg.2009.09.006; Wohrle J, 2010, AM J CARDIOL, V105, P804, DOI 10.1016-j.amjcard.2009.10.060; Wollert KC, 2004, LANCET, V364, P141, DOI 10.1016-S0140-6736(04)16626-9; Xing DQ, 2012, CIRCULATION, V125, P1533, DOI 10.1161-CIRCULATIONAHA.111.078436; Yao K, 2008, HEART, V94, P1147, DOI 10.1136-hrt.2007.137919; Yousef M, 2009, J AM COLL CARDIOL, V53, P2262, DOI 10.1016-j.jacc.2009.02.051; Zhang SN, 2009, CLIN CARDIOL, V32, P458, DOI 10.1002-clc.20575; Zoghbi GJ, 2006, J AM COLL CARDIOL, V47, P2296, DOI 10.1016-j.jacc.2005.11.0880
Hypoalbuminaemia and incident heart failure in older adults
No full textAims: To test the hypothesis that baseline hypoalbuminaemia is associated with incident heart failure (HF) in community-dwelling older adults. Methods and resultsOf the 5795 community-dwelling adults aged <65 years in the Cardiovascular Health Study, 5450 were free of centrally adjudicated prevalent HF at baseline, and also had data on baseline serum albumin. Of these, 599 (11) had hypoalbuminaemia, defined as baseline serum albumin levels ≤3.5 mg/dL. Propensity scores for hypoalbuminaemia were calculated for each patient and used to assemble a matched cohort of 582 pairs of participants with and without hypoalbuminaemia, who were well balanced on 58 baseline characteristics. Using Cox regression models, we estimated the association of hypoalbuminaemia with centrally adjudicated incident HF during 9.6 years of median follow-up. Matched participants had a mean (±SD) age of 74 (±6) years, 62 were women, and 16 were African Americans. Incident HF occurred in 25 and 20 of matched participants with and without hypoalbuminaemia, respectively [hazard ratio when hypoalbuminaemia was compared with normoalbuminaemia, 1.40; 95 confidence interval, 1.05-1.85; P = 0.020]. Pre-match unadjusted, multivariable-adjusted, and propensity-adjusted hazard ratios (95 confidence intervals) for incident HF associated with hypoalbuminaemia were 1.33 (1.12-1.58; P = 0.001), 1.33 (1.11- 1.60; P = 0.002), and 1.25 (1.04-1.50; P = 0.016), respectively. The combined endpoint of incident HF or all-cause mortality occurred in 59 and 50 of matched participants with and without hypoalbuminaemia, respectively (hazard ratio, 1.33; 95 confidence interval, 1.11-1.61; P = 0.002). ConclusionsAmong community-dwelling older adults without HF, baseline hypoalbuminaemia was associated with increased risk of incident HF during 10 years of follow-up. © The Author 2011
Myocardial perfusion in patients with a totally occluded left anterior descending coronary artery reinjected by a normal right coronary artery: The role of collateral circulation
No full textIn this article, myocardial perfusion in patients with a totally occluded left anterior descending artery reinjected by a normal right coronary artery is assessed using stress single photon emission computed tomography (SPECT). In all, 20 patients, with a totally occluded left anterior descending artery reinjected by normal right coronary artery, underwent myocardial single photon emission computed tomography imaging within 60 days of angiography. All patients had abnormal perfusion single photon emission computed tomography results and 70percent had reversible defects. Perfusion defects at rest were present in 75percent of patients, with perinecrotic residual ischemia in 45percent of patients whereas for 30percent of patients, no viable myocardium was detected in the collateral-dependent segments. In all, 25percent of patients had no resting perfusion defects but all are presented with stress-induced ischemia. Collaterals are not protective against stress-induced ischemia, but they can preserve myocardial viability. This conclusion is highly supported by the presence of residual ischemia in the collateral-dependent segments. © 2008 Sage Publications.Aboul-Enein F, 2004, J NUCL MED, V45, P950; AKUTSU Y, 1995, INT J CARDIOL, V51, P47, DOI 10.1016-0167-5273(95)02396-E; Eriksen UH, 2002, CLIN CARDIOL, V25, P340, DOI 10.1002-clc.4950250707; Fujita M, 2004, HEART, V90, P246, DOI 10.1136-hrt.2002.007989; Fukai M, 2000, J Cardiol, V35, P103; HABIB GB, 1991, CIRCULATION, V83, P739; He ZX, 2001, J NUCL CARDIOL, V8, P452, DOI 10.1067-mnc.2001.114799; ISKANDRIAN AS, 1982, CIRCULATION, V65, P242; Koerselman J, 2003, CIRCULATION, V107, P2507, DOI 10.1161-01.CIR.0000065118.99409.5F; KOLIBASH AJ, 1982, AM J CARDIOL, V50, P230; Lee CW, 2000, J AM COLL CARDIOL, V35, P949; MCFALLS EO, 1993, EUR HEART J, V14, P336; Nicolau JC, 1997, INT J CARDIOL, V61, P47, DOI 10.1016-S0167-5273(97)00134-4; NIENABER CA, 1990, AM J CARDIOL, V65, P991, DOI 10.1016-0002-9149(90)91002-N; Pohl T, 2001, J AM COLL CARDIOL, V38, P1872, DOI 10.1016-S0735-1097(01)01675-8; Popma J. J., 2001, HEART DIS TXB CARDIO, P387; SAMBUCETI G, 1995, J AM COLL CARDIOL, V26, P615, DOI 10.1016-0735-1097(95)00209-M; Schaper W, 2003, ARTERIOSCL THROM VAS, V23, P1143, DOI 10.1161-01.ATV.0000069625.11230.96; Tayebjee MH, 2004, QJM-INT J MED, V97, P259, DOI 10.1093-qjmed-hch053; TUBAU JF, 1981, AM J CARDIOL, V47, P27, DOI 10.1016-0002-9149(81)90285-X; VANOVERSCHELDE JLJ, 1993, CIRCULATION, V87, P1513; WAINWRIGHT RJ, 1980, BRIT HEART J, V43, P47; Werner GS, 2007, HEART, V93, P778, DOI 10.1136-hrt.2006.108159; Werner GS, 2005, AM HEART J, V149, P129, DOI 10.1016-j.ahj.2004.04.042; Werner GS, 2001, CIRCULATION, V104, P2784, DOI 10.1161-hc4801.10035252
Prognostic value of quantitative stress myocardial perfusion imaging in unstable angina patients with negative cardiac enzymes and no new ischemic ECG changes
No full textBackground. Limited data are available on the value of quantitative stress myocardial perfusion imaging (MPI) in patients with unstable angina. In this report we sought to study the long-term prognostic value of quantitative stress MPI in patients hospitalized with unstable angina with no new ischemic electrocardiographic changes and negative cardiac enzymes. Methods and results. The study population consisted of 136 patients who were hospitalized at the Methodist Hospital, Houston, Tex, with unstable angina and subsequently underwent MPI before discharge. Cox proportional hazards (regression) analysis was performed to identify clinical and MPI predictors of hard cardiac events (death or nonfatal myocardial infarction). During a mean follow-up of 31 ± 17 months, 20 patients (15percent) sustained either cardiac death (n = 12) or nonfatal myocardial infarction (n = 8). The significant multivariate predictors of cardiac events were the total perfusion defect size (P = .002), the presence of reversible perfusion defects (P = .01), and the presence of multiple perfusion defects (P = .03). The perfusion defect size was significantly larger in patients with events than in those without events (21percent ± 20percent vs 12percent ± 14percent, P = .002). Kaplan-Meier analysis showed that cardiac events were much more likely to develop in patients with defects involving 15percent or more of the left ventricle than in those with defects involving less than 15percent of the left ventricle (P = .003). Conclusions. In patients hospitalized with unstable angina with no new ischemic electrocardiographic changes and negative cardiac enzymes, quantitative stress MPI provides powerful prognostic information that can be used in the risk stratification of these patients. Copyright © 2005 by the American Society of Nuclear Cardiology.Wallentin L, 1999, LANCET, V354, P708; Braunwald E, 2000, J AM COLL CARDIOL, V36, P970, DOI 10.1016-S0735-1097(00)00889-5; Braunwald E, 2002, J AM COLL CARDIOL, V40, P1366, DOI 10.1016-S0735-1097(02)02336-7; BROWN KA, 1983, J AM COLL CARDIOL, V1, P994; BROWN KA, 1991, J AM COLL CARDIOL, V17, P1053; Cannon CP, 2001, NEW ENGL J MED, V344, P1879, DOI 10.1056-NEJM200106213442501; Dakik HA, 1996, CIRCULATION, V94, P2735; GIBSON RS, 1983, CIRCULATION, V68, P321; ISKANDRIAN AS, 1993, J AM COLL CARDIOL, V22, P665; Lee E., 1992, STAT METHODS SURVIVA; MAHMARIAN JJ, 1995, J AM COLL CARDIOL, V25, P1333, DOI 10.1016-0735-1097(95)00016-W; MAHMARIAN JJ, 1990, J AM COLL CARDIOL, V15, P318; STRATMANN HG, 1994, CIRCULATION, V89, P615; STRATMANN HG, 1995, AM J CARDIOL, V76, P236, DOI 10.1016-S0002-9149(99)80072-1; STRATMANN HG, 1995, AM HEART J, V130, P734, DOI 10.1016-0002-8703(95)90071-3; WACKERS FJ, 1999, ACC CURR J REV, V8, P65, DOI 10.1016-S1062-1458(99)00016-177
Regadenoson for myocardial perfusion imaging: Is it safe?
No full text[No abstract available]Abuin G, 2009, TEX HEART I J, V36, P8; AlJaroudi WA, 2013, EUR J NUCL MED MOL I, V40, P341, DOI 10.1007-s00259-012-2296-4; Ananthasubramaniam K, 2012, J NUCL CARDIOL, V19, P319, DOI 10.1007-s12350-011-9508-3; Andreassi MG, 2011, PHARMACOGENET GENOM, V21, P469, DOI 10.1097-FPC.0b013e328347d2c6; [Anonymous], 2014, J NUCL CARDIOL S1, V21; Bagley SJ, 2012, CARDIOL J, V19, P92, DOI 10.5603-CJ.2012.0016; Brinkert M, 2014, EUR J NUCL MED MOL I, V41, P511, DOI 10.1007-s00259-013-2619-0; CERQUEIRA MD, 1994, J AM COLL CARDIOL, V23, P384; Cerqueira MD, 2008, JACC-CARDIOVASC IMAG, V1, P307, DOI 10.1016-j.jcmg.2008.02.003; Dhalla AK, 2006, J PHARMACOL EXP THER, V316, P695, DOI 10.1124-jpet.105.095323; Doukky R, 2012, J NUCL CARDIOL, V19, P448, DOI 10.1007-s12350-012-9533-x; Doukky R, 2013, J NUCL CARDIOL, V20, P205, DOI 10.1007-s12350-012-9654-2; Gao ZH, 2001, J PHARMACOL EXP THER, V298, P209; Geleijnse ML, 1997, J AM COLL CARDIOL, V30, P595, DOI 10.1016-S0735-1097(97)00206-4; Gordi T, 2006, CLIN PHARMACOKINET, V45, P1201, DOI 10.2165-00003088-200645120-00005; Grady EC, 2011, J NUCL CARDIOL, V18, P521, DOI 10.1007-s12350-011-9373-0; Hage FG, 2009, AM HEART J, V157, P771, DOI 10.1016-j.ahj.2009.01.011; Hage FG, 2011, J NUCL CARDIOL, V18, P1086, DOI 10.1007-s12350-011-9429-1; Hsi DH, 2013, J NUCL CARDIOL, V20, P481, DOI 10.1007-s12350-013-9694-2; Hurle A, 2010, ANN THORAC SURG, V89, P38, DOI 10.1016-j.athoracsur.2009.10.008; Iskandrian AE, 2007, J NUCL CARDIOL, V14, P645, DOI 10.1016-j.nuclcard.2007.06.114; LETTE J, 1995, J NUCL CARDIOL, V2, P3, DOI 10.1016-S1071-3581(05)80003-0; Lieu HD, 2007, J NUCL CARDIOL, V14, P514, DOI 10.1016-j.nuclcard.2007.02.016; Minic Z, 2014, AUTON NEUROSCI-BASIC, V180, P32, DOI 10.1016-j.autneu.2013.10.005; Pandit A, 2012, J NUCL CARDIOL, V19, P1236, DOI 10.1007-s12350-012-9610-1; Parker MW, 2013, J NUCL CARDIOL, V20, P185, DOI 10.1007-s12350-012-9641-7; Partington SL, 2012, J NUCL CARDIOL, V19, P970, DOI 10.1007-s12350-012-9562-5; Prenner BM, 2012, J NUCL CARDIOL, V19, P681, DOI 10.1007-s12350-012-9547-4; Rosenblatt J, 2014, J NUCL CARDIOL; Ross MI, 2013, J NUCL CARDIOL, V20, P197, DOI 10.1007-s12350-013-9679-1; Saadjian AY, 2009, EUR HEART J, V30, P1510, DOI 10.1093-eurheartj-ehp126; Shah S, 2013, PHARMACOTHERAPY, V33, pe90, DOI 10.1002-phar.1238; Shryock JC, 1998, CIRCULATION, V98, P711; Sokol DK, 2013, BMJ-BRIT MED J, V347, DOI 10.1136-bmj.f6426; STUART RJ, 1980, CHEST, V77, P94, DOI 10.1378-chest.77.1.94; Yesil M, 2008, INT HEART J, V49, P525, DOI 10.1536-ihj.49.525; Zhao G, 2008, J CARDIOVASC PHARM, V52, P467, DOI 10.1097-FJC.0b013e31818e035b; Zoghbi GJ, 2012, J NUCL CARDIOL, V19, P126, DOI 10.1007-s12350-011-9474-91
Improvement of cardiac function in thalassemia major treated with L-carnitine
No full textIntroduction: Heart disease secondary to chronic anemia and hemosiderosis remains the major cause of morbidity and mortality in thalassemic patients. Chronic anemia and the tissue hypoxia it induces impair free fatty acid oxidation and ATP production in myocardial cells. The use of L-carnitine, a butyric acid derivative, may help overcome some of these defects. Objective: To investigate the effect of L-carnitine therapy on cardiac function in thalassemia major patients. Materials and Methods: Cardiac function was evaluated in 30 patients attending our clinic. The mean (±SD) age was 15.87 ± 3.19 years. The studies we performed included echocardiography, Doppler and multigated equilibrium radionuclide angiography (MUGA). Systolic and diastolic function was evaluated before starting L-carnitine treatment and after 6 months of oral L-carnitine (50 mg-kg-day). Results: Echocardiography studies revealed no significant changes in systolic and diastolic function after L-carnitine therapy (p 0.05). Analysis of the data taken by MUGA performed in 20 of the patients, however, showed a significant improvement of diastolic function after 6 months of L-carnitine therapy. The mean peak filling rate (end-diastolic volume-s) increased from 3.15 ± 1.06 to 3.61 ± 1.68 (p 0.03). The time to peak (during filling) decreased significantly from 143.45 ± 42.04 to 117.70 ± 24.40 s (p 0.02). Systolic function showed a significant increase in the left ventricular ejection fraction from 58.25 ± 9.92 to 63.95 ± 10.11percent (p = 0.0001). Conclusion: L-Carnitine may be an effective drug for improving the cardiac status of thalassemic patients. MUGA is the most accurate technique of those used here for assessing left ventricular function in these patients. Copyright © 2004 S. Karger AG, Basel.ALDOURI MA, 1990, ACTA HAEMATOL-BASEL, V84, P113; Anand I, 1998, CARDIOVASC DRUG THER, V12, P291, DOI 10.1023-A:1007721917561; Anderson LJ, 2002, LANCET, V360, P516, DOI 10.1016-S0140-6736(02)09740-4; Armitage P, 1994, STAT METHODS MED RES; BAHL VK, 1992, AM HEART J, V124, P1516, DOI 10.1016-0002-8703(92)90066-5; Colonna P, 2000, AM HEART J, V139, pS124, DOI 10.1067-mhj.2000.103918; CORR PB, 1989, J CLIN INVEST, V83, P927, DOI 10.1172-JCI113978; DESIDERI A, 1994, CAN J CARDIOL, V10, P93; FREEMAN AP, 1989, CLIN LAB HAEMATOL, V11, P299, DOI 10.1111-j.1365-2257.1989.tb00227.x; GottsaunerWolf M, 1996, EUR J NUCL MED, V23, P1613, DOI 10.1007-BF01249624; ISKANDRIAN AS, 1996, NUCL CARDIAC IMAGING; Jessup M, 1998, ANN NY ACAD SCI, V850, P242, DOI 10.1111-j.1749-6632.1998.tb10481.x; KONO T, 1992, CIRCULATION, V86, P1317; Kothari S S, 1998, Indian Heart J, V50, P59; KREMASTINOS DT, 1993, CIRCULATION, V88, P1127; KREMASTINOS DT, 1985, CARDIOLOGY, V72, P129, DOI 10.1159-000173853; Kucuk NO, 1999, ANN NUCL MED, V13, P175; LATTANZI F, 1993, CIRCULATION, V87, P748; LEVY WC, 1992, J NUCL MED, V33, P763; MCDONALD IG, 1976, CIRCULATION, V53, P860; Modell B, 2000, LANCET, V355, P2051, DOI 10.1016-S0140-6736(00)02357-6; OLIVIERI NF, 1994, NEW ENGL J MED, V331, P574, DOI 10.1056-NEJM199409013310903; PEPINE CJ, 1991, CLIN THER, V13, P2; PERRINE SP, 1993, NEW ENGL J MED, V328, P81, DOI 10.1056-NEJM199301143280202; Reich S, 2000, BLOOD, V96, P3357; SAU F, 1989, Cardiologia (Rome), V34, P221; Sotirakopoulos N, 2002, RENAL FAILURE, V24, P505, DOI 10.1081-JDI-120006777; SPIRITO P, 1990, CIRCULATION, V82, P188; Walter JH, 1996, ARCH DIS CHILD, V74, P475; Yesilipek MA, 1998, ACTA HAEMATOL-BASEL, V100, P162, DOI 10.1159-000040895; ZURLO MG, 1989, LANCET, V2, P2728191
Health status after invasive or conservative care in coronary and advanced kidney disease
No full textBACKGROUND In the ISCHEMIA-CKD trial, the primary analysis showed no significant difference in the risk of death or myocardial infarction with initial angiography and revascularization plus guideline-based medical therapy (invasive strategy) as compared with guideline-based medical therapy alone (conservative strategy) in participants with stable ischemic heart disease, moderate or severe ischemia, and advanced chronic kidney disease (an estimated glomerular filtration rate of <30 ml per minute per 1.73 m2 or receipt of dialysis). A secondary objective of the trial was to assess angina-related health status. METHODS We assessed health status with the Seattle Angina Questionnaire (SAQ) before randomization and at 1.5, 3, and 6 months and every 6 months thereafter. The primary outcome of this analysis was the SAQ Summary score (ranging from 0 to 100, with higher scores indicating less frequent angina and better function and quality of life). Mixed-effects cumulative probability models within a Bayesian framework were used to estimate the treatment effect with the invasive strategy. RESULTS Health status was assessed in 705 of 777 participants. Nearly half the participants (49%) had had no angina during the month before randomization. At 3 months, the estimated mean difference between the invasive-strategy group and the conservative-strategy group in the SAQ Summary score was 2.1 points (95% credible interval, −0.4 to 4.6), a result that favored the invasive strategy. The mean difference in score at 3 months was largest among participants with daily or weekly angina at baseline (10.1 points; 95% credible interval, 0.0 to 19.9), smaller among those with monthly angina at baseline (2.2 points; 95% credible interval, −2.0 to 6.2), and nearly absent among those without angina at baseline (0.6 points; 95% credible interval, −1.9 to 3.3). By 6 months, the between-group difference in the overall trial population was attenuated (0.5 points; 95% credible interval, −2.2 to 3.4). CONCLUSIONS Participants with stable ischemic heart disease, moderate or severe ischemia, and advanced chronic kidney disease did not have substantial or sustained benefits with regard to angina-related health status with an initially invasive strategy as compared with a conservative strategy
Management of coronary disease in patients with advanced kidney disease
No full textBACKGROUND Clinical trials that have assessed the effect of revascularization in patients with stable coronary disease have routinely excluded those with advanced chronic kidney disease. METHODS We randomly assigned 777 patients with advanced kidney disease and moderate or severe ischemia on stress testing to be treated with an initial invasive strategy consisting of coronary angiography and revascularization (if appropriate) added to medical therapy or an initial conservative strategy consisting of medical therapy alone and angiography reserved for those in whom medical therapy had failed. The primary outcome was a composite of death or nonfatal myocardial infarction. A key secondary outcome was a composite of death, nonfatal myocardial infarction, or hospitalization for unstable angina, heart failure, or resuscitated cardiac arrest. RESULTS At a median follow-up of 2.2 years, a primary outcome event had occurred in 123 patients in the invasive-strategy group and in 129 patients in the conservative-strategy group (estimated 3-year event rate, 36.4% vs. 36.7%; adjusted hazard ratio, 1.01; 95% confidence interval [CI], 0.79 to 1.29; P=0.95). Results for the key secondary outcome were similar (38.5% vs. 39.7%; hazard ratio, 1.01; 95% CI, 0.79 to 1.29). The invasive strategy was associated with a higher incidence of stroke than the conservative strategy (hazard ratio, 3.76; 95% CI, 1.52 to 9.32; P=0.004) and with a higher incidence of death or initiation of dialysis (hazard ratio, 1.48; 95% CI, 1.04 to 2.11; P=0.03). CONCLUSIONS Among patients with stable coronary disease, advanced chronic kidney disease, and moderate or severe ischemia, we did not find evidence that an initial invasive strategy, as compared with an initial conservative strategy, reduced the risk of death or nonfatal myocardial infarction
