40 research outputs found

    Reproducibility of left ventricular mass measurements by two-dimensional and M-mode echocardiography

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    AbstractBoth two-dimensional and M-mode echocardiography provide accurate estimates of left ventricular mass. However, their reproducibility in serial studies has not been compared, although this issue is critical to evaluation of regression of hypertrophy. To determine which technique provides more reproducible estimates of left ventricular mass, three serial studies were performed prospectively in each of eight normal adults over 5 months. Both two-dimensional and M-mode echocardiograms were obtained at each of these 24 studies. Measurements were performed by two independent observers who did not know patient identity. For the two-dimensional method, left ventricular mass was determined with use of a computer light-pen system and the truncated ellipsoid formula. For the M-mode method, mass was calculated from Penn convention measurements with use of the cube formula.At study 1 the group mean left ventricular mass by two-dimensional echocardiography (115 ± 20 g) did not differ from that by M-mode study (127± 37 g, p = NS). However, serial estimates of left ventricular mass were more reproducible by two-dimensional echocardiography. The mean difference among the three serial two-dimensional studies in each individual was 4.8 ± 4 g (4.2 ± 3%) by the two-dimensional method, but was 18.5 ± 13 g (14.9 ± 10%) by the M-mode method (p = 0.01). Interobserver results for left ventricular mass by two-dimensional echocardiography correlated closely (r = 0.95, n = 24, p < 0.001).The superior reproducibility of two-dimensional echocardiographic estimates of left ventricular mass in normal adults supports the use of two-dimensional echocardiography when serial studies are to be performed

    Selection of patients for heart transplantationin the current era of heart failure therapy

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    AbstractObjectivesWe sought to assess the relationship between survival, peak exercise oxygen consumption (Vo2), and heart failure survival score (HFSS) in the current era of heart failure (HF) therapy.BackgroundBased on predicted survival, HF patients with peak Vo2<14 ml/min/kg or medium- to high-risk HFSS are currently considered eligible for heart transplantation. However, these criteria were developed before the widespread use of beta-blockers, spironolactone, and defibrillators—interventions known to improve the survival of HF patients.MethodsPeak Vo2and HFSS were assessed in 320 patients followed from 1994 to 1997 (past era) and in 187 patients followed from 1999 to 2001 (current era). Outcomes were compared between these two groups of patients and those who underwent heart transplantation from 1993 to 2000.ResultsSurvival in the past era was 78% at one year and 67% at two years, as compared with 88% and 79%, respectively, in the current era (both p < 0.01). One-year event-free survival (without urgent transplantation or left ventricular assist device) was improved in the current era, regardless of initial peak Vo2: 64% vs. 48% for peak Vo2<10 ml/min/kg (p = 0.09), 81% vs. 70% for 10 to 14 ml/min/kg (p = 0.05), and 93% vs. 82% for >14 ml/min/kg (p = 0.04). Of the patients with peak Vo2of 10 to 14 ml/min/kg, 55% had low-risk HFSS and exhibited 88% one-year event-free survival. One-year survival after transplantation was 88%, which is similar to the 85% rate reported by the United Network for Organ Sharing for 1999 to 2000.ConclusionsSurvival for HF patients in the current era has improved significantly, necessitating re-evaluation of the listing criteria for heart transplantation

    Cell Tracking and the Development of Cell-Based Therapies A View From the Cardiovascular Cell Therapy Research Network

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    Cell-based therapies are being developed for myocardial infarction (MI) and its consequences (e.g., heart failure) as well as refractory angina and critical limb ischemia. The promising results obtained in preclinical studies led to the translation of this strategy to clinical studies. To date, the initial results have been mixed: some studies showed benefit, whereas in others, no benefit was observed. There is a growing consensus among the scientific community that a better understanding of the fate of transplanted cells (e.g., cell homing and viability over time) will be critical for the long-term success of these strategies and that future studies should include an assessment of cell homing, engraftment, and fate as an integral part of the trial design. In this review, different imaging methods and technologies are discussed within the framework of the physiological answers that the imaging strategies can provide, with a special focus on the inherent regulatory issues

    Impairment of subendocardial perfusion reserve and oxidative metabolism in nonischemic dilated cardiomyopathy.

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    BACKGROUND: Cardiac magnetic resonance (CMR) and [(11)C]acetate positron emission tomography (PET) were used to assess the hypothesis that patients with nonischemic dilated cardiomyopathy (NIDCM) have decreased subendocardial perfusion reserve and impaired oxidative metabolism, consistent with the concept of energy starvation in heart failure (HF). METHODS AND RESULTS: CMR myocardial perfusion was evaluated in 13 NIDCM patients and 15 control subjects with coronary risk factors and normal myocardial perfusion. The NIDCM patients underwent [(11)C]acetate PET. The myocardial perfusion index (MPI) was calculated as the normalized rate of myocardial signal augmentation following gadolinium contrast injection. Hyperemic transmural, subendocardial, and subepicardial MPI were reduced in NIDCM compared with control subjects [0.13 vs 0.18 (P \u3c .001), 0.13 vs 0.17 (P \u3c .001), and 0.13 vs 0.17 (P = .008), respectively]. The subendocardial perfusion reserve was 1.59 ± 0.21 vs 1.86 ± 0.32 for the subepicardium (P = .002), demonstrating reduced perfusion reserve. The myocardial oxidative metabolic rate (kmono) per unit demand (rate-pressure product) was reduced in proportion to perfusion reserve (P = .02) CONCLUSIONS: Impaired subendocardial perfusion reserve in NIDCM confirmed results previously attained only in animal models. Impaired perfusion and impaired oxidative metabolism are consistent with subendocardial energy starvation in HF

    Data from: High reproducibility of adenosine stress cardiac magnetic resonance myocardial perfusion imaging in patients with nonischemic dilated cardiomyopathy

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    Objective: To evaluate the reproducibility of first-pass contrast-enhanced cardiac MR (CMR) myocardial perfusion imaging in patients with non-ischaemic dilated cardiomyopathy (NIDCM). Design: Prospective observational study. Setting: Single centre, tertiary care hospital. Participants: 6 outpatient participants with NIDCM. Outcome: Reproducibility of semiquantitative myocardial perfusion analysis by CMR. Method: 6 patients with NIDCM were studied twice using first-pass of contrast transit through the left ventricular (LV) myocardium with a saturation-recovery gradient echo sequence at rest and during adenosine-induced hyperaemia. The anterior wall was divided into endocardial (Endo) and epicardial (Epi) segments. The Myocardial Perfusion Index (MPI) was calculated as the myocardial signal augmentation rate normalised to the LV cavity rate. The Myocardial Perfusion Reserve Index (MPRI) was calculated as hyperaemic/resting MPI. Results: Between study 1 and 2, median MPI was similar for resting Endo (0.076 vs 0.077), hyperaemic Endo (0.143 vs 0.143), resting Epi (0.073 vs 0.074), and hyperaemic Epi (0.135 vs 0.134). Median MPRI was similar for Endo (1.84 vs 1.87) and Epi (1.90 vs 2.00). Combining Endo and Epi MPI (N=12), there was excellent agreement between Study 1 and 2 for resting MPI (r=0.998, intraclass correlation coefficient (ICC) 0.998, coefficients of variation (CoV) 1.4%), hyperaemic MPI (r=0.979, ICC 0.963, CoV 3.3%) and MPRI (r=0.989, ICC 0.94, CoV 3.8%). Conclusions: Resting and hyperaemic myocardial perfusion using a normalised upslope analysis during adenosine CMR is a highly reproducible technique in patients with NIDCM. Trial registration number: Clinical Trials.Gov ID NCT00574119

    Multicenter, Randomized, Double-Blind, Placebo-Controlled Study on the Effect of Oral Tolvaptan on Left Ventricular Dilation and Function in Patients With Heart Failure and Systolic Dysfunction

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    Multicenter, Randomized, Double-Blind, Placebo-Controlled Study on the Effect of Oral Tolvaptan on Left Ventricular Dilation and Function in Patients With Heart Failure and Systolic Dysfunction James E. Udelson, Frank A. McGrew, Enrique Flores, Hassan Ibrahim, Stewart Katz, Gregory Koshkarian, Terrence O’Brien, Marvin W. Kronenberg, Christopher Zimmer, Cesare Orlandi, Marvin A. Konstam In a multicenter, randomized, double-blind, placebo-controlled trial in patients with heart failure and reduced left ventricular systolic function, 1 year of administration of tolvaptan 30 mg/day was studied to evaluate the effect on reducing left ventricular (LV) end-diastolic volume compared with placebo by using quantitative radionuclide ventriculography. A total of 240 patients were randomized. In a well-treated population of stable HF patients, LV volumes were stable during 1 year of follow-up. There was no significant effect of tolvaptan therapy on LV volumes observed during 1 year of therapy. Nonprespecified natural history data favored therapy with tolvaptan, with a reduction in the combined end point of mortality and heart failure hospitalization observed over the course of the trial. This study sought to examine the effects of vasopressin V2receptor antagonism with tolvaptan on the changes in left ventricular (LV) volumes over time. Vasopressin levels may be increased in patients with heart failure (HF) and may be a factor driving the progression of HF. This was a multicenter, randomized, double-blind, placebo-controlled trial conducted to evaluate the effect of long-term administration of the vasopressin V2-receptor antagonist tolvaptan (30 mg/day) on reducing left ventricular end-diastolic volume (LVEDV) compared with placebo in patients with HF and reduced systolic function, using quantitative radionuclide ventriculography at baseline, repeated after 1 year of therapy, and repeated again approximately 1 week after withdrawal of study drug. A total of 120 patients were randomized to tolvaptan and 120 were randomized to placebo. In the placebo group, there was no change in LVEDV over the course of follow-up (change of 0.0 ± 10.0 ml/m2). After 1 year of tolvaptan, there was a small reduction in LV volume (decrease of 1.8 ± 10.7 ml/m2); the between-group difference was not significant (p = 0.21). During the course of the trial, there were 6 deaths (5%) and 21 HF hospitalizations (18%) in the tolvaptan group, compared with 11 deaths (9%) and 34 HF hospitalizations (28%) in the placebo group. In a time-to-event analysis, there was a significant favorable effect of tolvaptan on the composite of mortality or heart failure hospitalization (p < 0.03 by log-rank test). In a well-treated population of stable HF patients, there was no significant effect of tolvaptan therapy on LV volumes observed during 1 year of therapy. Nonprespecified natural history data favored therapy with tolvaptan, with a reduction in the combined end point of mortality and heart failure hospitalization observed. (Multicenter, Randomized, Double-Blind, Placebo Controlled, Efficacy Study on the Effects of Tolvaptan on Left Ventricular Dilatation in Congestive Heart Failure Patients; http://clinicaltrials.gov/ct/show/NCT00043758?order=1; NCT00043758
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