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PubMed2002

Cardiac disease in transgenic mice expressing human immunodeficiency virus-1 nef in cells of the immune system.

We previously reported that a severe acquired immune deficiency syndrome-like disease develops in transgenic (Tg) mice expressing the human immunodeficiency virus-1 in its natural target cells: immature and mature CD4(+) T cells and cells of the macrophage/dendritic lineage. Here, we show that these mice also develop cardiac disease, characterized most prominently by a focal myocytolysis, occasionally by myocarditis and by deposition of endogenous immunoglobulin on cardiomyocytes. Microfil perfusion demonstrated widespread coronary arteriospasm and echocardiographic analysis revealed depressed cardiac function in Tg mice. A higher (but still modest) level of cardiomyocyte apoptosis was detected in Tg as compared to non-Tg hearts. Tg expression was detected in some of the infiltrating mononuclear cells, but not in cardiomyocytes or in cells of the heart vessels, suggesting a human immunodeficiency virus-1-induced disease process mediated by cells of the immune system. The similarity of the heart disease observed in these Tg mice to that observed in acquired immune deficiency syndrome patients suggests a common pathogenesis.

Animals↗
PubMed2000

A novel role for STAT3 in cardiac remodeling.

The binding of ligands to gp130 activates the JAK/STAT signal transduction pathway, where STAT3 plays a central role in transmitting signals from the membrane to the nucleus. STAT3 is essential for gp130-mediated cardiac myocyte hypertrophy. Cardiac-specific disruption of gp130 was shown to present heart failure in response to mechanical stress accompanied by an increase in apoptosis. Thus, the inactivation of STAT3 resulting from the loss of gp130 may be a key event in the transition from cardiac hypertrophy to heart failure. Proper vascular growth is essential for normal cardiac development and remodeling process. Recently, bcl-xL and VEGF have identified as target genes of STAT and together can promote cardiac myocyte survival by prevention of apoptosis and restoration of energy deprivation. In this review, STAT3 is highlighted as a regulator of angiogenic factors, and activation of STAT-mediated signaling in the cardiac myocyte is proposed as a novel therapeutic strategy for the prevention of heart failure.

Cytokines↗
PubMed2001

Oozing from the pericardium as an etiology of cardiac tamponade associated with screw-in atrial leads.

Screw-in atrial pacing leads are widely used. Cardiac tamponade is a complication. An 81-year-old woman with advanced atrioventricular block underwent permanent pacemaker implantation and subsequently developed cardiac tamponade. At surgery, the lead-tip screw was found penetrated through the right atrium but not through the pericardium. The source of bleeding was confirmed to scratching the inner pericardial membrane by the screw tip. Although cardiac tamponade due to perforation and leakage is known, tamponade caused by the trauma of an atrial screw on the pericardium with resultant ooze is less well described.

Aged↗
PubMed2006

Role of contrast-enhanced dobutamine stress echocardiography in predicting outcome in patients with known or suspected coronary artery disease.

Although the application of intravenous contrast agents during stress echocardiography has been shown to improve diagnostic accuracy for detecting coronary artery disease, less information exists regarding its prognostic value. The aim of this study was to determine the role of contrast-enhanced dobutamine stress echocardiography (DSE) for predicting future cardiac events in patients with coronary artery disease (CAD). We studied 893 patients (mean age: 66, 581 men) with known or suspected CAD undergoing contrast-enhanced DSE. Positivity was defined as new/worsened wall motion abnormality or fixed abnormality during stress. All patients were followed for 15 +/- 10 months to evaluate hard cardiac events (cardiac death and nonfatal myocardial infarction) and total cardiac events (hard cardiac events, congestive heart failure, unstable angina, and late revascularization). Three patients were lost to follow-up, and 128 patients developed cardiac events, including 21 hard cardiac events. The 3-year event free survival rate was significantly lower in patients with positive DSE results than in those with negative DSE results. Stepwise Cox multivariate analysis revealed that positivity of DSE (P < 0.0001, Hazard ratio (HR): 2.48) and peak wall motion score index (WMSI) >1.5 (P < 0.0001, HR: 2.41) were independent predictors for total cardiac events. Considering hard cardiac events, the independent predictors were peak WMSI > 1.5 (P < 0.0001, HR: 6.65) and age > 70 years (P < 0.005, HR: 3.27). We conclude that contrast-enhanced DSE provides important prognostic information for future cardiac events.

Adult↗
PubMed2002

Spinal cord ischemia associated with cardiac arrest.

Ischemic spinal cord damage from cardiac arrest is rare. A 48-year-old man underwent a straightforward retroperitoneal aortofemoral bypass operation. The following day, he developed cardiac arrest and was resuscitated successfully, but permanent paraplegia was observed soon afterwards.

Heart Arrest↗
PubMed1989

Interleukin-2 and lymphokine-activated killer cell therapy of solid tumors: analysis of toxicity and management guidelines.

The National Cancer Institute (NCI) Extramural IL2/LAK Working Group treated 93 patients with 114 cycles of high-dose intravenous (IV) interleukin-2 (IL-2) and lymphokine-activated killer (LAK) cells in three phase II trials. Thirty-six patients had metastatic melanoma, 35 had metastatic renal cell cancer, and 22 had colorectal cancer. All patients had a Karnofsky performance status greater than or equal to 80% and normal laboratory tests and organ function, and had received no more than one prior form of immunotherapy or chemotherapy. Objective responders were eligible to receive up to two additional courses of therapy at 12-week intervals. The most frequent toxicities were a capillary leak syndrome resulting in marked extravascular fluid shifts, and hypotension requiring treatment with large volumes of IV fluids and vasopressor agents. Laboratory and clinical evidence of hepatic and renal dysfunction were virtually universal. Intensive care-level support was routinely provided and the toxicity observations confirmed the need for this level of care. The life-threatening toxicities were cardiac and pulmonary. Five of the 27 patients who experienced significant respiratory compromise required intubation and mechanical ventilatory support. Twenty patients developed cardiac arrhythmias, the majority of which were supraventricular. There was a single episode of ventricular tachycardia requiring cardioversion. Four patients had transient cardiac ischemia, and an additional four had myocardial infarctions, one of which was fatal. With these exceptions, all toxicities were rapidly reversible. The occurrence of only a single therapy-related death and a very low incidence of other irreversible or life-threatening events is comparable to the level of toxicities often observed in other phase II trials. Although the intensity of this regimen limits this approach to a subset of cancer patients with excellent performance status and adequate organ function, because of the frequency and apparent durability of complete responses, this treatment warrants further investigation.

Adult↗
PubMed2004

Development-related changes in the expression of shear stress responsive genes KLF-2, ET-1, and NOS-3 in the developing cardiovascular system of chicken embryos.

Blood flow patterns play an important role in cardiovascular development, as changes can cause congenital heart malformations. Shear stress is positively correlated to blood flow. Therefore, it is likely that shear stress is also involved in cardiac development. In this study, we investigated the expression patterns of ET-1, NOS-3, and KLF-2 mRNA in a series of developmental stages of the chicken embryo. These genes are reported to be shear responsive. It has been demonstrated that KLF-2 is confined to areas of high shear stress in the adult human aorta. From in vitro studies, it is known that ET-1 is down-regulated by shear stress, whereas NOS-3 is up-regulated. Therefore, we expect ET-1 to be low or absent and NOS-3 to be high at sites where KLF-2 expression is high. Our study shows that, in the early stages, expression patterns are mostly not shear stress-related, whereas during development, this correlation becomes stronger. We demonstrate overlapping expression patterns of KLF-2 and NOS-3 in the narrow parts of the cardiovascular system, like the cardiac inflow tract, the atrioventricular canal, outflow tract, and in the early stages in the aortic sac and the pharyngeal arch arteries. In these regions, the expression patterns of KLF-2 and NOS-3 exclude that of ET-1. Our results suggest that, in the embryonic cardiovascular system, KLF-2 is expressed in regions of highest shear stress, and that ET-1 and NOS-3 expression, at least in the later stages, is related to shear stress.

Animals↗
PubMed1996

[Total repair of tetoralogy of Fallot in an adult: report of a case without prior treatment at 59 years of age].

We reported successful repair of tetoralogy of Fallot of a male case aged 59 years old. There was no palliative operation prior to this correction. The preoperative clinical features were as follows: dyspnea on effort and at rest, cyanosis and clubbing, multiple cerebral thrombosis without symptoms. Polycytemia was remarkable at Hb 23.3 g/dl and Ht 73.8%. PaO2 was 39.2 mmHg and hypoxemia was recognized. CTR was 59% and pulmonary vascular shadows were decreased but bilateral pulmonary arteries were well developed. Cardiac catheterization showed that high RV systolic pressure equal to that of LV and severe RV outflow obstruction. Pulmonary artery was well developed (the diameter ratio of PA and aorta: 0.84). Collateral arteries to the pulmonary vascular system were not significant by aortography. The surgical procedures were performed under conventional method. Pulmonary valvular stenosis was released by comissurotomy and RV outflow tract obstruction was also released through minimal right ventriculotomy. The conus branch of coronary artery crossed the outflow tract, so that we preserved this artery for preventing right ventricular failure post-operatively. There was no need to use trans-annular patch for reconstruction of the outflow tract. In post operative course, only a low dosage of catecholamin was required but no other special treatment was needed. Ventricular and supraventricular arrhythmia had appeared in short period but after administration of anti arrhythmic drugs, heart rhythm was converted to sinus rhythm easily. Pathological findings of RV muscle which resected at the operation showed marked fibrous degeneration and irregularity of cells, and it suggested that sever hypoxia and high pressure for long time affected the ventricular muscle. We concluded that even older patients of tetralogy of Fallot were corrected safely and were able to get good quality of life after operation.

Age of Onset↗
PubMed1995

Does concurrent or prior nicotine exposure interact with neonatal hypoxia to produce cardiac cell damage?

Cigarette smoking during pregnancy exposes the fetus to both nicotine and hypoxia/ischemia; postnatal exposure to second-hand smoke also involves substances that cause hypoxia (CO, HCN). Although developing cardiac cells are more resistant to hypoxia-induced damage than are mature cells, we examined whether nicotine affects this resistance, either when exposure is concurrent with hypoxia, or when animals are exposed to nicotine prenatally and receive subsequent hypoxic exposure. One, 8-, or 15-day-old rats exposed to 7% O2 for 2 hr all showed inhibition of cardiac DNA synthesis. By contrast, administration of nicotine at either low (0.3 mg/kg) or high (3 mg/kg) doses failed to alter DNA synthesis. To examine effects on cells that were not undergoing mitosis, we examined ornithine decarboxylase (ODC), an enzymatic marker for cell damage. One day old rats showed inhibition of ODC by hypoxia, a response that represents preservation of cell integrity; by 8 days of age, ODC was increased by hypoxia, evidence of cell damage. The high dose of nicotine evoked an increase in ODC at all ages and the low dose exacerbated the effects of hypoxia at 8 days of age. Prenatal nicotine exposure caused a transient inhibition of cardiac DNA synthesis but did not produce evidence of cell damage (ODC, protein synthesis markers) by itself, nor did it alter the effect of a subsequent postnatal exposure to hypoxia. These results suggest that cardiac cell damage could emerge as a consequence of concurrent, repeated exposures to nicotine and hypoxia. Such effects could contribute to the elevated incidence of perinatal morbidity/mortality and Sudden Infant Death Syndrome associated with smoking.

Analysis of Variance↗
PubMed2005

Cardiac tissue-specific repression of CELF activity disrupts alternative splicing and causes cardiomyopathy.

Members of the CELF family of RNA binding proteins have been implicated in alternative splicing regulation in developing heart. Transgenic mice that express a nuclear dominant-negative CELF protein specifically in the heart (MHC-CELFDelta) develop cardiac hypertrophy and dilated cardiomyopathy with defects in alternative splicing beginning as early as 3 weeks after birth. MHC-CELFDelta mice exhibit extensive cardiac fibrosis, severe cardiac dysfunction, and premature death. Interestingly, the penetrance of the phenotype is greater in females than in males despite similar levels of dominant-negative expression, suggesting that there is sex-specific modulation of splicing activity. The cardiac defects in MHC-CELFdelta mice are directly attributable to reduced levels of CELF activity, as crossing these mice with mice overexpressing CUG-BP1, a wild-type CELF protein, rescues defects in alternative splicing, the severity and incidence of cardiac hypertrophy, and survival. We conclude that CELF protein activity is required for normal alternative splicing in the heart in vivo and that normal CELF-mediated alternative splicing regulation is in turn required for normal cardiac function.

Alternative Splicing↗
PubMed2004

[Cardiac manifestations of Lyme borreliosis].

Lyme borreliosis is increasing in Poland in both incidence and recognition with 655 cases reported in 1997 and 3574 in 2003. Approximately 4% of patients will develop cardiac manifestations--the least well documented complication of Lyme disease. Cardiac involvement usually occurs within weeks to months of the infecting tick bite and includes varying degrees of atrioventricular block as the commonest manifestation and tachyarrhythmias, myopericarditis, mild cardiac muscle dysfunction. There has been evidence that long standing dilated cardiomyopathy may be associated with chronic Borrelia burgdorferi infection. Patients with atrioventricular block have good prognosis. Most cases resolve within 1 to 2 weeks. Temporary, but almost never permanent, cardiac pacing may be required for some patients. Cardiac manifestations of Lyme disease are treatable with antibiotics. Lyme carditis should be taken into consideration in patients with acute as well as chronic heart diseases.

Arrhythmias, Cardiac↗
PubMed1996

Prognosis among patients with out-of-hospital cardiac arrest judged as being caused by deterioration of obstructive pulmonary disease.

AIM: To describe the prognosis of patients with out-of-hospital cardiac arrest judged to be caused by the deterioration of obstructive pulmonary disease. PATIENTS: All patients in the community of Göteborg Sweden who suffered out-of-hospital cardiac arrest between 1980 and 1992 attended by our emergency medical service and in whom cardiopulmonary resuscitation was initiated. METHODS: The etiology of cardiac arrest was determined according to clinical history, observations at resuscitation and findings at autopsy. RESULTS: There were 3434 cardiac arrests of which 130 (4%) were judged to have been caused by deterioration of obstructive pulmonary disease. Of these patients 50% were found in asystole, 40% in pulseless electrical activity, and only 7% in ventricular fibrillation. Among patients with cardiac arrest caused by obstructive pulmonary disease 21 (16%) were hospitalized alive and six (5%) were discharged from hospital. Among patients who developed cardiac arrest after arrival of the ambulance, 16% were discharged from hospital versus 0% among patients who had arrest prior to arrival of the ambulance. CONCLUSION: Among patients with out-of-hospital cardiac arrest caused by deterioration of obstructive pulmonary disease, half were found in asystole. Overall, the survival rate was low. This highlights the importance of effective treatment early in the course of deterioration of obstructive pulmonary disease in order to avoid cardiac arrest.

Adult↗
PubMed2000

Apoptosis-related genes expressed in cardiovascular development and disease: an EST approach.

Apoptosis (programmed cell death) is an important process which, in conjunction with cell proliferation, maintains cell number homeostasis. Although apoptosis has been more extensively investigated in other tissues [1,2], only recently has this process been suspected as a significant contributor to both disease and normal development of the cardiovascular system [3-6]. Grasping a comprehension of the underlying genetic mechanisms of apoptosis is especially crucial considering that cardiac myocytes irreversibly exit the cell cycle and thus fail to proliferate during pathological conditions. Despite great strides in understanding the molecular pathways of apoptosis, there still remain numerous questions to be answered. Identifying key genes that are involved in the regulatory process of apoptosis in the cardiovascular system will serve as a basis for creating more effective therapeutic treatments in cardiovascular disease and provide an understanding of how cardiac development is modulated. This review provides a brief summary of recent data implicating genes that may be involved in apoptosis in the cardiovascular system. It also outlines the continued usefulness of large-scale generation of expressed sequence tags (ESTs) to establish expression profiles from the cardiovascular system and as a means of identifying potentially significant apoptotic regulators previously characterized in other tissues but not as yet in the cardiovascular system.

Animals↗
PubMed2000

Regulation of MEF2 by p38 MAPK and its implication in cardiomyocyte biology.

Myocyte enhancer factor-2 (MEF2), transcription factors and mitogen-activated protein kinase (MAPK) p38 are regulators of cardiac development and various pathophysiologic processes. The recent finding that p38 can directly regulate MEF2 transcription factors suggests a novel mechanism for reprogramming cardiac gene expression in response to neuroendocrine and/or stress stimulation. This review weighs the accumulating evidence for a p38 MAPK-MEF2 signal transduction cascade and discusses its role in cardiac myocyte biology.

Animals↗
PubMed1999

Cardiac ion channels and antihistamines: possible mechanisms of cardiotoxicity.

Despite the enormous success of second generation antihistamines, in the mid-1980s, about 10 years after their introduction in the market, several reports appeared in the literature indicating the rare occurrence of a form of polymorphic ventricular dysrhythmia, the 'torsade de pointes', after the administration of astemizole or terfenadine. This cardiac side-effect has been interpreted as a consequence of the interference of these drugs with cardiac K+ channels involved in action potential repolarization, and in particular with the IKr component of the cardiac repolarizing current. As the K+ channels encoded by the human ether-a-gogo-related gene (HERG) seem to represent the molecular basis of IKr, this cardiac K+ channel was soon recognized as a primary target for second generation antihistamine-induced proarrhythmic effects. In fact, both terfenadine and astemizole have been shown to block HERG K+ channels in a concentration range similar to that found in the plasma of subjects with cardiotoxic manifestations. However, no correlation can be found between the ability to prolong the cardiac action potential duration and the H1-antagonistic activity by several antihistamines, suggesting that HERG blockade and cardiotoxic potential are not class properties of second generation antihistamines. In fact, other molecules such as cetirizine, loratadine, acrivastine, and fexofenadine seem to lack both cardiotoxic potential and HERG-blocking ability at therapeutically relevant concentrations. The marked heterogeneity displayed by second generation antihistamines in their ability to prolong the cardiac action potential duration and to block HERG K+ channels might be of considerable therapeutical significance for those patients at risk of developing cardiac dysrhythmias and in need of therapy with H1-receptor blockers; it also emphasizes the importance of an evaluation of the possible blockade of HERG K+ channels during the early developmental phases of novel compounds belonging to this therapeutical class.

Cation Transport Proteins↗
PubMedDate not supplied

Blastoderm degeneration, an early embryonic failure in dwarf Single Comb White Leghorn chickens.

Blastoderm degeneration is an early embryonic lethal condition observed in selected paired matings within a line of dwarf Single Comb White Leghorn chickens that results in a 25% reduction of the hatch of fertilized eggs. The disorder is macroscopically evident at 32 h of incubation by the presence of a small localized indentation on the outer periphery of the expanding blastoderm. The affected blastoderms undergo a series of rapid macroscopic degenerative changes that conclude at about 120 h characterized by the presence of dispersed blastoderm fragments on the surface of the egg's yolk. Microscopically, this embryonic failure appears to manifest itself between Hamburger-Hamilton stages 8 and 9 of development and is characterized by a series of retarded developmental processes: closure of the anterior neuropore, brain vesicle differentiation, somite formation, and cardiac development. The disorder is inherited as an autosomal recessive trait. Attempts to identify factors that influence the disorder have thus far been unsuccessful. The symbol bld is proposed for this recessive gene.

Animals↗
PubMed1998

"Conventional" antihistamines slow cardiac repolarization in isolated perfused (Langendorff) feline hearts.

We examined the effects of "conventional" antihistamines on cardiac repolarization by using the isolated perfused feline heart model. Representative drugs from the major classes of antihistamines were tested. Each of the antihistamines evaluated in this study elicited a dose-dependent slowing of cardiac repolarization, as indicated by the QT prolongations observed from electrocardiogram (ECG) tracings recorded during these experiments. The concentrations of drugs tested ranged from 1 to 30 microM. Of the drugs analyzed, clemastine and hydroxyzine appeared to be the most potent (relative EC50 values, 5.2 and 6.6 microM, respectively), causing the QT to lengthen by as much as 40-50% at a concentration of 10 microM. Brompheniramine, chlorpheniramine, and diphenhydramine displayed intermediate potencies with respect to QT prolongation (relative EC50 values, 11-13 microM), whereas cyproheptadine, chlorcyclizine, and promethazine were the least potent of the antihistamines tested (relative EC50 values, 16-20 microM). It is concluded that the antihistamines evaluated in this study act directly on the heart to slow cardiac repolarization. These findings could have important clinical relevance for patients taking excessive dosages of conventional antihistamines and those at risk of developing cardiac arrhythmias.

Animals↗
PubMed2005

Comparison of serum cardiac troponin T and creatine kinase MB isoenzyme mass concentrations in asphyxiated term infants during the first 48 h of life.

OBJECTIVE: This prospective study aimed to compare serum creatine kinase MB isoenzyme (CK-MB) mass concentrations and cardiac troponin T (cTnT) concentrations during the first 48 h of life in asphyxiated term infants. METHODS: Serum cTnT and CK-MB mass concentrations of 50 term infants with clinical features of perinatal asphyxia were measured at birth and at 12, 24 and 48 h of age by chemiluminescence immunoassay. These infants were followed up until discharge or death. Cord blood CK-MB and cTnT concentrations of 50 healthy term infants were also assayed. RESULTS: At birth, asphyxiated infants had significantly higher concentrations of cTnT and CK-MB than controls (P < 0.0001). Serum cTnT of asphyxiated infants with low ejection fraction <60% was significantly higher at 12 and 24 h than those with normal ejection fraction (P < 0.05). Asphyxiated infants with congestive cardiac failure had significantly higher serum cTnT concentration during the first 48 h of life than those without congestive cardiac failure (P or= 0.1). CONCLUSION: Unlike CK-MB, serum cTnT concentrations are significantly higher in asphyxiated infants who die or develop cardiac dysfunction.

Asphyxia Neonatorum↗