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The use of stem cells has proved to be an important tool in investigating the events of early cardiac development, differentiation, and morphogenesis. In addition, stem cell transplantation in the treatment of certain cardiac disorders has shown early promise. We have attempted to present a balanced review of both basic studies and clinical-therapeutic potential of stem cells transplantation in the damaged heart.
BACKGROUND: Survival after surgical embolectomy for massive postcesarean pulmonary embolism causing sustained cardiac arrest is rare. CASE: One day after an uneventful cesarean delivery, a woman developed cardiac asystole and apnea due to pulmonary embolism. Femoral-femoral cardiopulmonary bypass performed during continuous cardiopulmonary resuscitation allowed a successful embolectomy. Upon awakening, the patient reported a near-death experience. Pulmonary embolism causes approximately 2 deaths per 100,000 live births per year in the United States, and postcesarean pulmonary embolism is probably more common than pulmonary embolism after vaginal delivery. CONCLUSION: Massive pulmonary embolism is a potentially treatable catastrophic event after cesarean delivery, even if continuous cardiopulmonary resuscitation is required until life-saving embolectomy is done.
Two patients are described who exhibited cardiac complications during administration of etomidate. One patient showed myocardial ischaemia and the other developed cardiac asystole.
OBJECTIVE: The aim of this study was to identify the mode of presentation of patients with clinical anastomotic leaks following restorative colorectal resection for carcinoma. PATIENTS AND METHODS: Prospective information was collected on all patients having restorative resection of colorectal cancer. These data were reviewed for a five-year period (1994-1998) to identify all patients who had suffered a clinical anastomotic leak and their notes were retrieved and reviewed. RESULTS: Three hundred and seventy-nine patients underwent restorative resection for colorectal cancer during the study period (178 female, 201 male), mean age 70 years (range 36-94). There were 22 (6%) clinical anastomotic leaks. Seven (32%) patients presented with obvious abdominal peritonitis. The remaining 15 (68%) were initially misdiagnosed. Thirteen (59%) patients were treated for cardiac symptoms, 1 (5%) patient for obstruction and 1 (5%) for ascites. The delay in diagnosis ranged from 0 to 11 days (mean 4 days). For the whole series of 379 there were 30 patients who suffered cardiac symptoms (8%) 13(43%) of whom had an anastomotic leak. CONCLUSION: Patients who develop cardiac symptoms following restorative colorectal resection for carcinoma should have a water soluble enema as there is a 40% chance that they will have an anastomotic leak.
We have previously shown that 1 h of maternal insulin-induced hypoglycemia is teratogenic to rat embryos during the initial stages of neurulation, when they are dependent on uninterrupted glycolysis (day 9.5-9.7 of development). To determine whether this vulnerability persists in later stages of neural tube and cardiac development, we infused insulin into 16 conscious pregnant rats for 1 h beginning after embryos had developed the capacity for aerobic glucose metabolism (day 10.6 of development). Half of the pregnant animals were allowed to become hypoglycemic (44 +/- 2 mg/dl) during the insulin infusions. The other half received glucose infusions to maintain normoglycemia (130 +/- 3 mg/dl). Normal plasma glucose levels were maintained in all animals after the insulin infusions. Embryos were examined on day 11.5 of development. At that time, 1 of 111 embryos from the normoglycemic group and 1 of 109 embryos from the hypoglycemic group were grossly malformed (P greater than .5). Means of embryo crown-rump length (4.15 +/- 0.03 vs. 4.14 +/- 0.03 mm), somite number (29.7 +/- 0.1 vs. 29.8 +/- 0.2), and total protein content (320 +/- 5 vs. 326 +/- 6 micrograms) were also similar in the two groups (P greater than .5). Thus, we could not detect an embryotoxic effect of 1 h of maternal insulin-induced hypoglycemia beginning at day 10.6 of development. This finding is in contrast to our prior demonstration that a similar period of hypoglycemia occurring earlier in neurulation (day 9.7) caused growth retardation and developmental anomalies in embryos.(ABSTRACT TRUNCATED AT 250 WORDS)
We have used antibodies specific for troponin I proteins to examine human cardiac development and have detected a transiently expressed developmental isoform. This isoform is distinct from adult cardiac troponin I (TnIc) but is indistinguishable, on the basis of electrophoretic mobility and antibody reactivity, from the isoform found in slow skeletal muscle (TnIs). Furthermore, we show that mRNA for TnIs is present in fetal, but not adult, heart. Analysis of a developmental series of fetal samples indicates that there is a transition in expression from TnIs to TnIc which occurs between 20 weeks fetal and 9 months postnatal development.
Sixty-eight determination of in vivo insulin resistance were conducted in 35 males (aged 29-63 yr) by measurement of steady-state plasma glucose levels during a combined intravenous infusion of propranolol, epinephrine, glucose, and insulin. Subjects were mildly diabetic and/or hyperlipidemic. All were asymptomatic, denied taking medication, and had no history of cardiac disease. All had normal resting electrocardiograms. During the infusion, mean increases in systolic and diastolic blood pressure were 27 +/- 12.2 (x +/- SD) and 14 +/- 5.7 mm Hg, respectively; mean reduction in heart rate was 19 +/- 6.1 beats/min. Six out of the 35 subjects developed cardiac arrhythmias during the infusion test. Maximal exercise treadmill tests failed to predict all subjects who subsequently developed arrhythmias during the infusion test. These results suggest that this infusion test should be performed under continuous cardiac monitoring and promptly terminated if major arrhythmias develop.
Although perioperative myocardial infarction has a relative low incidence, its occurrence is associated with a high morbidity and mortality. Although many single risk factors for developing a perioperative myocardial infarction have been described, it soon became apparent that surgical risk could hardly be determined by one single factor. A multifactorial approach for the preoperative assessment of patients at risk for developing cardiac complications in association with surgery and anesthesia was introduced. Further investigation, however, indicated that the risk of developing a perioperative myocardial infarction was not only determined by preoperative risk factors and a number of peroperative risk factors were also identified. Since identification of those patients, particularly at risk for developing a perioperative myocardial infarction, is a matter of prime importance in the choice of the treatment and the monitoring, a thorough understanding and knowledge of the different pre- and peroperative risk factors is a must for every surgeon and anesthetist.
Retinoic acid, the biologically active form of vitamin A, is a critical player in normal development. The concentration of retinoic acid is highly regulated by the embryo to prevent either a deficit or an excess of this molecule, conditions that have been shown to produce cardiac defects that vary depending on the severity and the timing of the insult. The vast majority of these defects are associated with the valves or the membranous septa of the heart, suggesting a problem with the formation of the cardiac mesenchyme from both within and outside the heart. While the exact role of retinoic acid in cardiac development is not known, it is believed that retinoic acid influences development by up- or down-regulating cardiac specific genes. This review briefly discusses the role of cardiac mesenchyme and cardiac neural crest in septation of the heart. This is followed by a discussion of vitamin A metabolism and the cardiac defects associated with abnormal levels of retinoic acid. Finally, a mechanism is proposed concerning the ways abnormal levels of retinoic acid lead to similar cardiac defects by disrupting the production of the extracellular matrix.
[Met5]-enkephalin, encoded by the preproenkephalin (PPE) gene, serves as a growth factor (opioid growth factor, OGF) during cardiac development in addition to its role as a neuroregulator. This study examined the ontogeny and relationship of gene and peptide expression in the mammalian heart during late embryonic, preweaning, and postweaning periods. Values for PPE mRNA of hearts in rats from embryonic day 16 (E16) to postnatal day 1 were 33 to 50% of levels found in adults. Adult values for the mature heart were comparable to those in the caudate, an area of the rat brain rich in PPE mRNA. Message gradually decreased during the first postnatal week to 10% of adult values and remained so until weaning. PPE mRNA on days 35 and 50 were three- and sevenfold, respectively, higher than at 21 days, and in adults was more than 50% greater than at day 50. Message for PPE in neonatal heart was regulated rapidly and in a sustained fashion by excess opioid agonist (OGF) or blockade of opioid-receptor interaction. [Met5]-enkephalin levels increased sevenfold between E18 and E20, and another 1.6-fold until birth. Having reached a zenith in the neonate, values for enkephalin-like peptide decreased gradually through the 2nd postnatal week, and were extremely low in adulthood. Indeed, a 43-fold difference in peptide levels was detected between neonatal and adult rat heart. These data provide evidence for the expression of a tightly regulated and distinct growth factor (OGF) during the crucial periods of cell proliferation and differentiation in the mammalian heart, and reveal that the source of OGF is autocrine and/or paracrine.
UNLABELLED: There is increasing evidence showing that inflammation is involved in heart failure. However, heart failure may differ greatly due to different aetiologies. The role of inflammation in hypertensive heart failure, particularly in the early stage of cardiac dysfunction, has not been studied completely. This study aims at finding out whether inflammation is involved in the early stage of heart dysfunction due to hypertension. METHODS: Ten spontaneously hypertensive rats (SHR) and ten age-matched Wistar rats were used. Cardiac morphology and function, as well as coronary flow reserve, were examined by echocardiography. mRNAs for cytokines and brain natriuretic peptide were determined by RT-PCR. RESULTS: The results demonstrate cardiac hypertrophy with increased heart/body weight ratio in SHR. Echocardiographic examination has shown that SHR developed diastolic heart dysfunction as determined by tissue Doppler without decrease in systolic function. In heart biopsies, there were increased mRNA levels for interleukin-6 and brain natriuretic peptide whereas decreased mRNA for interleukin-2, beta adrenergic receptor, interferon and NFkb in SHR as compared to WKY group. Coronary flow remained unchanged in both groups. CONCLUSION: SHR developed cardiac hypertrophy complicated with diastolic heart dysfunction with increased expression of brain natriuretic peptide, down-regulation of beta adrenergic receptors and simultaneous up-regulation of IL-6, which indicates active proinflammatory process as, at least partly, underlying mechanism during the early stage when cardiac hypertrophy associated with diastolic dysfunction occurs.
Recent evidence suggests that mutant huntingtin protein-induced energetic perturbations contribute to neuronal dysfunction in Huntington's disease (HD). Given the ubiquitous expression of huntingtin, other cell types with high energetic burden may be at risk for HD-related dysfunction. Early-onset cardiovascular disease is the second leading cause of death in HD patients; a direct role for mutant huntingtin in this phenomenon remains unevaluated. Here we tested the hypothesis that expression of mutant huntingtin is sufficient to induce cardiac dysfunction, using a well-described transgenic model of HD (line R6/2). R6/2 mice developed cardiac dysfunction by 8 weeks of age, progressing to severe failure at 12 weeks, assessed by echocardiography. Limited evidence of cardiac remodeling (e.g. hypertrophy, fibrosis, apoptosis, beta(1) adrenergic receptor downregulation) was observed. Immunogold electron microscopy demonstrated significant elevations in nuclear and mitochondrial polyglutamine presence in the R6/2 myocyte. Significant alterations in mitochondrial ultrastructure were seen, consistent with metabolic stress. Increased cardiac lysine acetylation and protein nitration were observed and were each significantly associated with impairments in cardiac performance. These data demonstrate that mutant huntingtin expression has potent cardiotoxic effects; cardiac failure may be a significant complication of this important experimental model of HD. Investigation of the potential cardiotropic effects of mutant huntingtin in humans may be warranted.
PURPOSE OF THE REVIEW: The fields of pediatric and congenital cardiac interventions continue to expand at a rapid pace. The last few years have witnessed a tremendous explosion in procedures such as the transcatheter closure of secundum atrial septal defects, patent foramen ovale, patent ductus arteriosus, stent placement for pulmonary artery stenosis, and coarctation of the aorta. The purpose of this review is to highlight important publications in the last year and the direction the field is taking. RECENT FINDINGS: Research data over the last year has concentrated on six main themes: (a) mid-to-long-term data for device closure of atrial septal defects, the incidence of late cardiac erosions, thrombus formation and heart block; (b) the transcatheter closure of muscular ventricular septal defects; (c) the transcatheter closure of perimembranous ventricular septal defects; (d) the placement of bioprosthetic valves in the pulmonary and aortic positions; (e) the 'hybrid' approach that combines surgical and interventional techniques in the management of various congenital cardiac defects; and (f) fetal interventions. SUMMARY: This review outlines the key data presented in the literature involving interventional cardiology for pediatric and congenital cardiac defects over the last year. It illustrates that in close collaboration with industry, together with bioengineers and cardiothoracic surgeons, adult cardiac interventionists and perinatologists should continue to expand the role of pediatric catheter interventions. Fetal interventions have the potential to alter the natural history of abnormal cardiac development.
Coronary sinus pacing was evaluated in 10 pigs during propoxyphene-induced cardiac failure. From baseline, propoxyphene chloride 15 mg . min-1 was infused until circulatory shock developed. Cardiac pacing was evaluated at different dose levels expressed as % of the shock dose of propoxyphene: at intoxication levels below 50% of the shock dose, cardiac pacing improved cardiac performance. At dose levels above 50% of the shock dose cardiac performance deteriorated further during pacing. The results are consistent with a severe negative inotropic effect of propoxyphene in overdose.
AIM: To investigate effects of icariin on cardiac gene expression and the modulation of nitric oxide (NO) signal transduction during the differentiation of embryonic stem (ES) cells into cardiomyocytes in vitro. METHODS: The expression levels of cardiac developmental-dependent genes were measured using reverse transcription-polymerase chain reaction (RT-PCR). The chronotropic responses of cardiomyocytes to b-adrenoceptor stimulation were determined. The levels of cAMP and cGMP in ES cells were measured using radioimmunoassay. Endogenous NO levels were measured by using the Griess reaction. Aminoguanidine (AG) was used to confirm the influence of icariin on the endogenous NO signal pathway. RESULTS: Icariin significantly elevated mRNA levels of cardiac transcription factors GATA4 and Nkx2.5, and cardiac-specific alpha-MHC, MLC-2v and beta-AR genes in a concentration- and time-dependent manner (P<0.05). Cardiomyocytes derived from embryoid body (EB) treated with icariin were more sensitive to isoprenaline (P<0.01). Treatment of ES cells with icariin resulted in a continued elevation in the cAMP/cGMP ratio before a shift to the cardiomyocyte phenotype (P<0.05). AG decreased the NO level, and delayed and decreased the incidence of contracting EB to only approximately 35% on d 5+11, an effect that could be rescued by icariin. When cells were cocultured with icariin and AG, the percentage of beating EB reached a peak level of 73% on d 5+11 (P<0.05). CONCLUSION: The inducible effects of icariin were partly related to increase in the expression of cardiac developmental-dependent genes, and elevation of the cAMP/cGMP ratio in ES cells, as well as upregulation of endogenous NO generation during the early stages of cardiac development.
Tight transcriptional control of foreign genes introduced into the germline of transgenic mice would be of great experimental value in studies of gene function. To develop a system in which the spatial and temporal expression of candidate genes implicated in cardiac development or function could be tightly controlled in vivo, we have generated transgenic mice expressing a tetracycline-controlled transactivator (tTA) under the control of a rat alpha myosin heavy chain promoter (MHC alpha-tTA mice), as well as mice harboring a candidate target gene implicated in the control of differentiation, Id1 (tet-Id1 mice). No expression of the target transgene was detected in any tissues of hemizygous tet-Id1 mice. Genetic crosses with MHC alpha-tTA mice resulted in transactivation of the Id1 transgene, but expression was restricted to heart, where tTA was expressed. Furthermore, transactivation of the target gene was tightly and reversibly controlled by systemic therapy with tetracycline, both in utero and postnatally. These studies demonstrate the feasibility of such a binary approach for tightly controlling the timing and extent of expression of transgenes in vivo. This approach should be generally useful for the ectopic expression of candidate genes in selected tissues during delineated developmental stages.
UNLABELLED: From Jan-21-91 to Jan-8-92 we performed percutaneous transvenous mitral commissurotomy (PTCM) with a Medi-tech balloon catheter (MBC) in 41 patients bearing mitral stenosis simple o predominant. We utilized an anterograde transseptal approach in order to access the mitral valve, the procedure failed in 5 patients, in 30 of them we used double MBC and single MBC were utilized in 6 patients. Both left ventriculogram and hemodynamic parameters were taken before and after PTCM. Posterior to PTCM an important decrease appeared in the mitral transvalvular gradient from 20.6 +/- 2.7 to 2.4 +/- 1.7 mmHg (p < 0.0001) and an average pressure of pulmonary artery of 46.2 +/- 9.8 to 23.9 +/- 6 mmHg (p < 0.0001), and also the pulmonary arterial resistance from 1178.1 to 557.1 dinas/cm-5/seg. There was an important concomitant increase in mitral valvular area from 0.84 +/- 0.11 to 2.38 +/- 0.08 cm2 (p < 0.0001) and in cardiac rate from 2.7 +/- 0.7 to 2.9 +/- 0.52 L/min (p < 0.001). COMPLICATIONS: Two female patients developed cardiac tamponade, one of them the procedure was successful, and for the other it was decided to submit her to valvular replacement. Mitral insufficiency was present in three patients; GI/IV in two of them and GII/IV angiographic in one. Another patient presented cerebral thromboembolism with complete recovery within 15 days. Short left to right shunt was detected only in 8 patients being 1.2/1 in 6 of them, 1.3/1 in one and 1.4/1 in other patient. Thirty three uncomplicated were dismissed within a maximum of 48 hours after procedure.(ABSTRACT TRUNCATED AT 250 WORDS)
A review is presented of the mechanisms that mediate the increase in cardiac mass that occurs in patients with hypertrophic cardiomyopathy. This increase in mass is mediated by an increase in the total mass of the myocytes and the total mass of interstitial fibrous connective tissue. The increase in myocyte mass is the most important of these two components. However, it is not clear at the present time whether this increase is mediated not only by an increase in the size of the cells (hypertrophy), but also by an increase in the numbers of myocytes (hyperplasia) or by a combination of these two factors. Hyperplasia normally occurs during the prenatal phase of cardiac development and stops soon after birth, at which time hypertrophy becomes the main mechanism by which cardiac mass increases. Under certain circumstances, the ability of cardiac myocytes to synthesize DNA and undergo mitotic division can be restored; however, it is uncertain to what extent this results in complete cell division or only in either polyploidy or bi- or multinucleation. It is proposed that in hypertrophic cardiomyopathy, increased hyperplasia of cardiac myocytes occurs early in life and leads to permanently disturbed patterns of cardiac gross anatomy; it is then followed by a phase of progressive hypertrophy after the switch from hyperplastic to hypertrophic growth. It is possible that hyperplasia continues to occur after the usual time of this switch. It is also proposed that the increased number of layers of myocytes in the ventricular septum of patients with hypertrophic cardiomyopathy is a consequence of exaggerated hyperplasia during development.