Quantitation of myocardial 99mTc-HMDP uptake with new SPECT/CT cadmium zinc telluride (CZT) camera in patients with transthyretin-related cardiac amyloidosis: Ready for clinical use?

BACKGROUND: The aim of this study was to investigate the feasibility of assessing absolute myocardial 99mTc-HMDP uptake in patients with suspected cardiac ATTR using SUV with a whole-body CZT SPECT-CT camera (DNM670CZT). METHODS: Fifteen patients with suspected cardiac ATTR (Perugini ≥ 2) underwent a conventional 99mTc-HMDP planar imaging and a thoracic SPECT/CT using a DNM 670CZT. A control group consisted of 15 patients with negative scintigraphy (Perugini < 2). SUVmax (mg·L-1) and percentage of injected dose (%ID) were calculated in a cardiac volume of interest (VOI) encompassing the left ventricle. VOIs were also placed in the lung, the right pectoris major, and the sternum. A heart-to-lung SUVmax ratio (HLR) was calculated. RESULTS: All ATTR patients demonstrated an increased cardiac HMDP SUVmax (12.2 ± 3.7 mg·L-1) vs controls (3.5 ± 1.2, P < .0001). Percentage of ID, pectoral uptake and HLR were significantly higher in the ATTR group (1.1 ± 0.3 vs 0.15 ± 0.8, P < .0001; 1.5 ± 0.3 vs 0.9 ± 0.3, P < .0001; 9.7 ± 3 vs 4.3 ± 2.2, P < .0001). Bone uptake was not statistically different between the two groups. CONCLUSION: This study demonstrated the feasibility of quantitative 99mTc-HMDP SUVmax measurement using a whole-body SPECT/CT CZT camera in patients with suspected cardiac ATTR.

First Follow-Up of Cardiac Amyloidosis Treated by Tafamidis, Evaluated by Absolute Quantification in Bone Scintigraphy.

Assessment of absolute myocardial hydroxydimethylene diphosphonate-technetium-99m uptake using standardized uptake value with a single-photon emission computed tomography-computed tomography cadmium zinc telluride camera (Discovery NM/CT 670CZT, GE Healthcare, Chicago, Illinois) in a patient with cardiac transthyretin-related amyloidosis treated with tafamidis showed a decrease in hydroxydimethylene diphosphonate cardiac uptake. This imaging technique should be helpful in monitoring therapy and evaluating prognosis. (Level of Difficulty: Intermediate.).

Heart Transplantation for Peripartum Cardiomyopathy: A Single-Center Experience / Transplante Cardíaco por Cardiomiopatia Periparto: Uma Experiência de Centro Único

Abstract Background: Peripartum cardiomyopathy is an idiopathic disorder defined by the occurrence of acute heart failure during late pregnancy or post-partum period in the absence of any other definable cause. Its clinical course is variable and severe cases might require heart transplantation. Objective: To investigate long-term outcomes after heart transplantation (HT) for peripartum cardiomyopathy (PPCM). Methods: Out of a single-center series of 1938 HT, 14 HT were performed for PPCM. We evaluated clinical characteristics, transplant-related complications, and long-term outcomes, in comparison with 28 sex-matched controls. Primary endpoint was death from any cause; secondary endpoints were transplant-related complications (rejection, infection, cardiac allograft vasculopathy). A value of p < 0.05 was considered of statistical significance. Results: PPCM patients and matched controls were comparable for most variables (all p values > 0.05), except for a higher use of inotropes at the time of HT in PPCM group (p = 0.03). During a median follow-up of 7.7 years, 16 patients died, 3 (21.5%) in PPCM group and 13 (46.5%) in control group. Mortality was significantly lower in PPCM group (p = 0.03). No significant difference was found in terms of transplant-related complications (p > 0.05). Conclusions: Long-term outcomes following HT for PPCM are favorable. Heart transplantation is a valuable option for PPCM patients who did not recover significantly under medical treatment.

Resumo Fundamento: A cardiomiopatia periparto é uma doença idiopática definida pela ocorrência de insuficiência cardíaca aguda durante a gravidez tardia ou pós-parto na ausência de qualquer outra causa definível. Seu curso clínico é variável e casos graves podem exigir transplante. cardíaco. Objetivo: Pesquisar os resultados a longo prazo após transplante cardíaco (TC) por cardiomiopatia periparto (CMPP). Métodos: De uma única série central de 1938 TC, 14 TC foram realizados por CMPP. Foram avaliadas características clínicas, complicações relacionadas ao transplante e resultados a longo prazo, em comparação com 28 controles pareados por gênero. O principal critério de avaliação foi a morte por qualquer causa; os critérios secundários foram complicações relacionadas ao transplante (rejeição, infecção, vasculopatia do aloenxerto cardíaco). Um valor de p < 0,05 foi considerado estatisticamente significante. Resultados: As pacientes com CMPP e controles pareados foram comparáveis ​​para a maioria das variáveis (todos os valores de p > 0,05), exceto para um maior uso de inotrópicos no momento do TC no grupo CMPP (p = 0,03). Durante um seguimento médio de 7,7 anos, 16 pacientes morreram, 3 (21,5%) no grupo CMPP e 13 (46,5%) no grupo controle. A mortalidade foi significativamente menor no grupo CMPP (p = 0,03). Não foram encontradas diferenças significativas em termos de complicações relacionadas ao transplante (p> 0,05). Conclusões: Os resultados a longo prazo após TC para CMPP são favoráveis. O transplante cardíaco é uma opção valiosa para pacientes com CMPP que não se recuperaram significativamente sob tratamento médico.

Von Willebrand Factor Multimers during Transcatheter Aortic-Valve Replacement.

BACKGROUND: Postprocedural aortic regurgitation occurs in 10 to 20% of patients undergoing transcatheter aortic-valve replacement (TAVR) for aortic stenosis. We hypothesized that assessment of defects in high-molecular-weight (HMW) multimers of von Willebrand factor or point-of-care assessment of hemostasis could be used to monitor aortic regurgitation during TAVR. METHODS: We enrolled 183 patients undergoing TAVR. Patients with aortic regurgitation after the initial implantation, as identified by means of transesophageal echocardiography, underwent additional balloon dilation to correct aortic regurgitation. HMW multimers and the closure time with adenosine diphosphate (CT-ADP), a point-of-care measure of hemostasis, were assessed at baseline and 5 minutes after each step of the procedure. Mortality was evaluated at 1 year. A second cohort (201 patients) was studied to validate the use of CT-ADP in order to identify patients with aortic regurgitation. RESULTS: After the initial implantation, HMW multimers normalized in patients without aortic regurgitation (137 patients). Among the 46 patients with aortic regurgitation, normalization occurred in 20 patients in whom additional balloon dilation was successful but did not occur in the 26 patients with persistent aortic regurgitation. A similar sequence of changes was observed with CT-ADP. A CT-ADP value of more than 180 seconds had sensitivity, specificity, and negative predictive value of 92.3%, 92.4%, and 98.6%, respectively, for aortic regurgitation, with similar results in the validation cohort. Multivariable analyses showed that the values for HMW multimers and CT-ADP at the end of TAVR were each associated with mortality at 1 year. CONCLUSIONS: The presence of HMW-multimer defects and a high value for a point-of-care hemostatic test, the CT-ADP, were each predictive of the presence of aortic regurgitation after TAVR and were associated with higher mortality 1 year after the procedure. (Funded by Lille 2 University and others; ClinicalTrials.gov number, NCT02628509.).

[Peripartum cardiomyopathy]. / Cardiomyopathie du péripartum.

The peripartum cardiomyopathy is a rare form of dilated cardiomyopathy resulting from alteration of angiogenesis toward the end of pregnancy. The diagnosis is based on the association of clinical heart failure and systolic dysfunction assessed by echocardiography or magnetic resonance imaging. Diagnoses to rule out are myocardial infarction, amniotic liquid embolism, myocarditis, inherited cardiomyopathy, and history of treatment by anthracycline. Risk factors are advance maternal age (>30), multiparity, twin pregnancy, African origin, obesity, preeclampsia, gestational hypertension, and prolonged tocolytic therapy. Treatment of acute phase is identical to usual treatment of acute systolic heart failure. After delivery, VKA treatment should be discussed in case of systolic function <25% because of higher risk of thrombus. A specific treatment by bromocriptine can be initiated on a case-by-case basis. Complete recovery of systolic function is observed in 50% of cases. The mortality risk is low. Subsequent pregnancy should be discouraged, especially if systolic function did not recover.

Alterations in neutrophil production and function at an early stage in the high-fructose rat model of metabolic syndrome.

BACKGROUND: Although neutrophils are crucially involved in inflammation, they have received only little attention in metabolic syndrome (MetS). We hypothesized that neutrophil infiltration into adipose tissue (AT) may occur at an early stage of MetS, in association with modulation of major functions of neutrophils and of their bone marrow production. METHODS: Fifty-six male Sprague-Dawley rats were fed regular (control rats (CRs)) or high-fructose (60%; fructose-fed rats (FFRs)) diets. After 6 weeks, metabolic parameters were measured. Distribution of neutrophils into AT was investigated by immunohistochemistry. Function of circulating neutrophils (activation, reactive oxygen species production, phagocytosis, and apoptosis) was determined by flow cytometry. Granulopoiesis was evaluated by measuring the number and survival characteristics of neutrophil progenitors using bone marrow culture assays and flow cytometry. RESULTS: Compared with the CR group, the FFR group developed MetS (i.e., arterial hypertension, hypertriglyceridemia, fasting hyperglycemia, and greater intra-abdominal AT volume) and presented higher neutrophil infiltration into AT. At resting state, no significant difference for circulating neutrophil functions was observed between the 2 groups. In contrast, circulating neutrophils from the FFR group exhibited higher responses to phorbol-12-myristate-13-acetate for all studied functions, compared with the CR group, suggesting that early MetS induces neutrophil priming. In parallel, a diminished clonal capacity and an increased apoptosis in bone marrow-derived granulocyte progenitors and neutrophil precursors were observed in the FFR group compared with the CR group. CONCLUSIONS: These results provide evidence of an increased infiltration into intra-abdominal AT and modified production, function, and phenotype of neutrophils at an early stage of high-fructose diet-induced MetS.

Segmental and global left ventricular function assessment using gated SPECT with a semiconductor Cadmium Zinc Telluride (CZT) camera: phantom study and clinical validation vs cardiac magnetic resonance.

BACKGROUND: We evaluated gated-SPECT using a Cadmium-Zinc-Telluride (CZT) camera for assessing global and regional left ventricular (LV) function. METHODS: A phantom study evaluated the accuracy of wall thickening assessment using systolic count increase on both Anger and CZT (Discovery 530NMc) cameras. The refillable phantom simulated variable myocardial wall thicknesses. The apparent count increase (%CI) was compared to the thickness increase (%Th). CZT gated-SPECT was compared to cardiac magnetic resonance (CMR) in 27 patients. Global and regional LV function (wall thickening and motion) were quantified and compared between SPECT and CMR data. RESULTS: In the phantom study using a 5-mm object, the regression between %CI and %Th was significantly closer to the line of identity (y = x) with the CZT (R (2) = 0.9955) than the Anger (R (2) = 0.9995, P = .03). There was a weaker correlation for larger objects (P = .003). In patients, there was a high concordance between CZT and CMR for ESV, EDV, and LVEF (all CCC >0.80, P < .001). CZT underestimated %CI and wall motion (WM) compared to CMR (P < .001). The agreement to CMR was better for WM than wall thickening. CONCLUSION: The Discovery 530NMc provided accurate measurements of global LV function but underestimated regional wall thickening, especially in patients with increased wall thickness.

The presence of apoptotic bone marrow cells impairs the efficacy of cardiac cell therapy.

Injection of autologous bone marrow cells into infarcted myocardium has been proposed to limit the deterioration of cardiac function following myocardial infarction (MI); unfortunately, the beneficial effects observed have been modest. One of the limiting factors is believed to be poor local survival of the injected cells, but the potential impact of apoptosis among the injected cells has yet to be assessed. Therefore, this study aimed to quantify the apoptosis rate in bone marrow mononuclear cells (BMMCs) prepared for cardiac therapy, and to analyze their effects in vitro on cardiomyoblast apoptosis and in vivo on cardiac function recovery following MI. Using rabbit BMMCs prepared by Ficoll gradient, apoptotic cells were detected via Annexin V (AnV) staining. The effects of depleting the apoptotic cell population by means of AnV magnetic beads was tested in vitro after coculture with cardiomyoblasts (H9c2 cells) and in vivo after cell injection into the infarcted area. Left ventricular ejection fraction and scar extent were assessed by echography and histology 2 months later. After Ficoll gradient isolation, 37.3% (33.4-37.9%) of BMMCs were found to be apoptotic (Apo(Base) BMMCs). AnV depletion decreased the proportion of apoptotic cells to 20% (17.6-32%) (Apo(Low) BMMCs). Rabbits treated in vivo with Apo(Low) BMMCs after MI presented with significantly improved left ventricular ejection fraction [41.4% (41.0-43.6%) vs. 34.6% (34.6-35.9%), p = 0.03), reduced scar extent [20.4% (17.9-24.3%) vs. 25.6% (17.9-27.9%), p = 0.057], and reduced rate of cardiomyocyte apoptosis compared to those treated with Apo(Base) BMMCs. H9c2 apoptosis was found to be higher after coculture with Apo(Base) than with Apo(Low) BMMCs [25.6% (22.6-29.6%) vs. 10.1% (6.6-12.6%), p = 0.03], a result partially reproduced by cocultures with microparticle-rich supernatants from BMMCs. The presence of apoptotic cells among BMMCs impairs the efficacy of cardiac cell therapy after MI, an effect possibly mediated by apoptotic microparticles.

Intracoronary autologous mononucleated bone marrow cell infusion for acute myocardial infarction: results of the randomized multicenter BONAMI trial.

AIMS: Intracoronary administration of autologous bone marrow cells (BMCs) leads to a modest improvement in cardiac function, but the effect on myocardial viability is unknown. The aim of this randomized multicentre study was to evaluate the effect of BMC therapy on myocardial viability in patients with decreased left ventricular ejection fraction (LVEF) after acute myocardial infarction (AMI) and to identify predictive factors for improvement of myocardial viability. METHODS AND RESULTS: One hundred and one patients with AMI and successful reperfusion, LVEF ≤45%, and decreased myocardial viability (resting Tl201-SPECT) were randomized to either a control group (n = 49) or a BMC group (n = 52). Primary endpoint was improvement of myocardial viability 3 months after AMI. Baseline mean LVEF measured by radionuclide angiography was 36.3 ± 6.9%. Bone marrow cell infusion was performed 9.3 ± 1.7 days after AMI. Myocardial viability improved in 16/47 (34%) patients in the BMC group compared with 7/43 (16%) in the control group (P = 0.06). The number of non-viable segments becoming viable was 0.8 ± 1.1 in the control group and 1.2 ± 1.5 in the BMC group (P = 0.13). Multivariate analysis including major post-AMI prognostic factors showed a significant improvement of myocardial viability in BMC vs. control group (P = 0.03). Moreover, a significant adverse role for active smoking (P = 0.04) and a positive trend for microvascular obstruction (P = 0.07) were observed. CONCLUSION: Intracoronary autologous BMC administration to patients with decreased LVEF after AMI was associated with improvement of myocardial viability in multivariate-but not in univariate-analysis. A large multicentre international trial is warranted to further document the efficacy of cardiac cell therapy and better define a group of patients that will benefit from this therapy. CLINICAL TRIAL REGISTRATION INFORMATION: URL: http://www.clinicaltrials.gov. Unique identifier NCT00200707.

Second successful surgical ventricular reconstruction: a cardiac magnetic resonance imaging illustration.

This case reports a magnetic resonance imaging (MRI) illustration of a successful ventricular reconstruction of a left ventricle pseudoaneurysm that developed four months after postmyocardial infarction ventricular repair. Thus, preoperative non-invasive MRI techniques are valuable diagnostic tools in this setting. Indeed, the present case shows that MRI greatly helped in the management and surgical decision-making.

Effects of trimetazidine, a partial inhibitor of fatty acid oxidation, on ventricular function and survival after myocardial infarction and reperfusion in the rat.

Trimetazidine (TMZ), a partial inhibitor of fatty acid oxidation, has been effective in treating chronic angina, but its effects on the development of post-myocardial infarction (MI) left ventricular remodeling are not defined. In this study, we tested whether chronic pre-MI administration of TMZ would be beneficial during and after acute MI. Two-hundred male Wistar rats were studied in four groups: sham + TMZ diet (n = 20), sham + control diet (n = 20), MI + TMZ diet (n = 80), and MI + control diet (n = 80) splitted into one short-term and one long-term experiments. Sham surgery consisted of a thoracotomy without coronary ligation. MI was induced by coronary occlusion followed by reperfusion. Left ventricle (LV) function and remodeling were assessed by serial echocardiography throughout a 24-week post-MI period. LV remodeling was also assessed by quantitative histological analysis of post-MI scar formation at 24 weeks post-MI. During the short-term experiment, 10/80 rats died after MI, with no difference between groups (MI + control = 7/40, MI + TMZ = 3/40, P = 0.3). In the long-term experiment, the deaths occurred irregularly over the 24 weeks with no difference between groups (MI + control = 16% mortality, MI + TMZ = 17%, P = 0.8). There was no difference between groups as regard to LV ejection fraction (MI + control = 36 +/- 13%, MI + TMZ = 35 +/- 13%, P = 0.6). In this experimental model, TMZ had no effects on the post-MI occurrence of LV dysfunction or remodeling. Further investigations are warranted to assess whether the partial inhibition of fatty acid oxidation may limit the ability of the heart to respond to acute severe stress.

Inhibition of tissue factor-factor VIIa proteolytic activity blunts hepatic metastasis in colorectal cancer.

BACKGROUND: Expression of the principal initiator of coagulation, tissue factor (TF), by colorectal cancer (CRC) cells is involved in tumoral angiogenesis and metastasis progression, after binding of factor VIIa (FVIIa) to TF and generation of TF-FVIIa activity. We thus hypothesized that inhibition of the TF pathway by active site-blocked FVIIa (FFR-FVIIa) may prevent the development of hepatic metastasis in CRC. METHODS: Rat tumoral cells (DHDK12 proB cells) expressing high levels of TF were injected in the portal vein in syngenic BDIX rats. Rats received intraperitoneal injection of either FFR-FVIIa, from d 3 to d 7 (adjuvant treatment) (n = 19), or solvent buffer (n = 18) (control group). Additionally, cancer cells were infused subcutaneously in 20 other rats, which were assigned to FFR-FVIIa adjuvant treatment (n = 10), or buffer treatment (n = 10). Macroscopic and histological analysis was performed at d 14. RESULTS: In the control group, infusion of cancer cells resulted in development of macroscopic hepatic tumors in 17/18 rats. In the adjuvant FFR-FVIIa group, macroscopic hepatic tumors were visible on the liver surface in 3/19 rats (P = 0.002 versus control). All rats with subcutaneous injection of proB cells exhibited macroscopic tumors, with no significant difference between the control and the treated ones. CONCLUSION: Inhibition of the proteolytic activity of TF-FVIIa complex blunted hematogenous hepatic metastasis, suggesting that TF-FVIIa is a relevant target for the prevention of hepatic metastasis in CRC. TF-blocking agents should be investigated as adjuvant treatment in this setting.

Role of the ATP-binding cassette transporter Abcg2 in the phenotype and function of cardiac side population cells.

Recently, the side population (SP) phenotype has been introduced as a reliable marker to identify subpopulations of cells with stem/progenitor cell properties in various tissues. We and others have identified SP cells from postmitotic tissues, including adult myocardium, in which they have been suggested to contribute to cellular regeneration following injury. SP cells are identified and characterized by a unique efflux of Hoechst 33342 dye. Abcg2 belongs to the ATP-binding cassette (ABC) transporter superfamily and constitutes the molecular basis for the dye efflux, hence the SP phenotype, in hematopoietic stem cells. Although Abcg2 is also expressed in cardiac SP (cSP) cells, its role in regulating the SP phenotype and function of cSP cells is unknown. Herein, we demonstrate that regulation of the SP phenotype in cSP cells occurs in a dynamic, age-dependent fashion, with Abcg2 as the molecular determinant of the cSP phenotype in the neonatal heart and another ABC transporter, Mdr1, as the main contributor to the SP phenotype in the adult heart. Using loss- and gain-of-function experiments, we find that Abcg2 tightly regulates cell fate and function. Adult cSP cells isolated from mice with genetic ablation of Abcg2 exhibit blunted proliferation capacity and augmented cell death. Conversely, overexpression of Abcg2 is sufficient to enhance cell proliferation, although with a limitation of cardiomyogenic differentiation. In summary, for the first time, we reveal a functional role for Abcg2 in modulating the proliferation, differentiation, and survival of adult cSP cells that goes beyond its distinct role in Hoechst dye efflux.

Comparison of blood activation in the wound, active vent, and cardiopulmonary bypass circuit.

BACKGROUND: During cardiopulmonary bypass, aspirated blood exhibits strong activation features, but the triggering event remains unclear. Contact of blood with the pericardial cavity and surgical wound has been advocated as the main trigger, but suction forces are also considered as a possible contributor. We thus designed a study to identify the possible causes involved in this activation. METHODS: In 10 patients, we analyzed hemostasis activation markers and inflammatory mediators in blood collected in the pericardial cavity and in blood actively aspirated from the left ventricle without any contact with the pericardial cavity. In addition, the same variables were determined in blood sampled in the cardiopulmonary bypass circuit. RESULTS: Markers of tissue factor pathway activation and of thrombin generation, microparticles, free hemoglobin, interleukin 6, and tumor necrosis factor-alpha were significantly increased in pericardial samples as compared with the left ventricle and cardiopulmonary bypass circuit samples. All measured variables were similar between left ventricle and cardiopulmonary bypass samples, except free hemoglobin, interleukin 6, and microparticle levels, which were significantly higher in the left ventricle. CONCLUSIONS: Blood contact with the pericardial cavity induces strong hemolysis, inflammatory mediator release, and coagulation activation, driven by tissue factor pathway activation. By contrast, suction forces applied to left ventricular blood poorly contribute to blood trauma and activation. Comparison of pericardial and left ventricular blood shows that contact with the pericardial cavity, and not suction forces, is the leading cause of blood activation. The specific trigger for blood trauma and activation present in the pericardial cavity remains to be identified.

The bone marrow--cardiac axis of myocardial regeneration.

Congestive heart failure remains the leading cause of morbidity and mortality in the developed world. Current therapies do not address the underlying pathophysiology of this disease, namely, the progressive loss of functional cardiomyocytes. The notion of repairing or regenerating lost myocardium via cell-based therapies remains highly appealing. The recent identification of adult stem cells, including both cardiac stem/progenitor cells and bone marrow stem cells, has triggered an explosive interest in using these cells for physiologically relevant cardiomyogenesis. Enthusiasm for cardiac regeneration via cell therapy has further been fueled by the many encouraging reports in both animals and human studies. Further intensive research in basic science and clinical arenas are needed to make this next great frontier in cardiovascular regenerative medicine a reality. In this review, we focus on the role of bone marrow-derived stem cells and cardiac stem/progenitor cells in cardiomyocyte homeostasis and myocardial repair and regeneration, as well as provide a brief overview of current clinical trials using cell-based therapeutic approaches in patients with heart disease.

In vivo autologous recellularization of a tissue-engineered heart valve: are bone marrow mesenchymal stem cells the best candidates?

OBJECTIVE: Bone marrow stem cells, especially the mesenchymal stem cell subpopulation, have been used to create in vitro tissue-engineered heart valves. We hypothesized that autologous bone marrow cells, injected in a decellularized porcine scaffold before surgical implantation, could promote in vivo recolonization and limit valve deterioration. We thus analyzed the effects of in situ injection of autologous bone marrow mononuclear cells and of mesenchymal stem cells on the outcome of xenogenic decellularized scaffolds in a lamb model. METHODS: Decellularized porcine pulmonary valves were implanted in the pulmonary artery under cardiopulmonary bypass in 14 lambs after injection in the scaffold of autologous bone marrow mononuclear cells (BMMC) group (n = 7) or of mesenchymal stem cells (MSC) group (n = 7). At 4 months, valve function was evaluated by echocardiography, and valves were explanted for macroscopic and histologic analysis. RESULTS: Mean transvalvular and distal gradients (millimeters of mercury) were lower in the MSC than those in the BMMC group (1.3 +/- 0.39 vs 4.24 +/- 0.91 and 4.05 +/- 1.89 vs 12.02 +/- 6.95, respectively; P < .02). Histologic examination showed significant recolonization and re-endothelialization in both groups. However, significant valve thickening and inflammatory cell infiltration were observed in the BMMC group. By contrast, valves from the MSC group displayed extracellular matrix and cell disposition close to those of native pulmonary valves. CONCLUSIONS: Tissue-engineered heart valves created from mesenchymal stem cells, injected directly in a decellularized xenograft scaffold, exhibited satisfactory hemodynamic and histologic aspects after 4 months. Further long-term studies are needed to demonstrate the potential of mesenchymal stem cells for clinical application in heart valve surgery.

Diagnosis, imaging, and treatment of an unusual cardiac hydatid cyst.

Echinococcosis is endemic in sheep- and cattle-raising areas in Europe, especially in Southern and Central Europe. In France, most cases originated from immigrants from countries where echinococcosis is endemic. Extremely rare native cases have been reported during the last few years in France, especially those concerning isolated cardiac hydatid cyst. In this case report, we propose a complete imaging description of the features of a typical cardiac hydatid cyst from cardiac MRI, complete with surgery, parasitology, and anatomopathology images.

The impact of the AMPD1 gene polymorphism on exercise capacity, other prognostic parameters, and survival in patients with stable congestive heart failure: a study in 686 consecutive patients.

BACKGROUND: Previous studies have demonstrated that the adenosine monophosphate deaminase 1 (AMPD1) C34T polymorphism may be associated with survival in cardiac populations with a protective effect of the T allele. However, these studies included limited number of patients with few cardiovascular events. METHODS: We prospectively analyzed the impact of the C34T polymorphism of the AMPD1 gene in 686 unrelated white patients with stable congestive heart failure related to left ventricular systolic dysfunction. Patients underwent echocardiography, radionuclide angiography, and a cardiopulmonary exercise test. Blood samples were drawn for standard and hormonal determinations and for genetic analysis. RESULTS: There were 517 (75%) CC homozygotes, 155 (23%) CT heterozygotes, and 14 (2%) TT mutated homozygotes. We did not demonstrate any impact of this polymorphism on clinical, biologic, echocardiographic, radionuclide, and exercise parameters in the whole population and in ischemic and nonischemic subgroups of patients. During a median follow-up period of 3 years, there were 145 cardiac-related deaths and 6 urgent transplantations. There was no impact of this polymorphism on survival. CONCLUSIONS: In our population, we did not demonstrate any effect of the C34T polymorphism of the AMPD1 gene on major congestive heart failure parameters and on survival.

Restoration of cardiac progenitor cells after myocardial infarction by self-proliferation and selective homing of bone marrow-derived stem cells.

Tissue-specific progenitor cells contribute to local cellular regeneration and maintain organ function. Recently, we have determined that cardiac side-population (CSP) cells represent a distinct cardiac progenitor cell population, capable of in vitro differentiation into functional cardiomyocytes. The response of endogenous CSP to myocardial injury, however, and the cellular mechanisms that maintain this cardiac progenitor cell pool in vivo remain unknown. In this report we demonstrate that local progenitor cell proliferation maintains CSP under physiologic conditions, with little contribution from extracardiac stem cell sources. Following myocardial infarction in adult mice, however, CSP cells are acutely depleted, both within the infarct and noninfarct areas. CSP pools are subsequently reconstituted to baseline levels within 7 days after myocardial infarction, through both proliferation of resident CSP cells, as well as through homing of bone marrow-derived stem cells (BMC) to specific areas of myocardial injury and immunophenotypic conversion of BMC to adopt a CSP phenotype. We, therefore, conclude that following myocardial injury, cardiac progenitor cell populations are acutely depleted and are reconstituted to normal levels by both self-proliferation and selective homing of BMC. Understanding and enhancing such processes hold enormous potential for therapeutic myocardial regeneration.