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PubMed1983

Cardiovascular features of 11 patients with eosinophilic endomyocardial disease.

This report describes the clinical features, cardiac investigations and treatment of eleven patients with biventricular eosinophilic endomyocardial disease, who were followed up for a mean of 3.2 years. Three patients died. Five patients presented with heart disease and hypereosinophilia. Six other patients presented with hypereosinophilia and developed cardiac disease later. Histological studies showed early acute necrotic lesions in five patients, later thrombotic lesions in one and late fibrotic lesions in three patients. Endomyocardial biopsy was the method of choice for diagnosing early acute necrotic and thrombotic lesions. Late fibrotic lesions were best shown by amplitude processed 2D echocardiography and angiocardiography. Episodes of heart failure responded well to treatment with prednisolone which appeared to inhibit progression of heart disease in two patients. Three patients with severe ventricular disease and valvular regurgitation responded well to surgical treatment. This longitudinal study has shown that eosinophilic endomyocardial disease can now be investigated and treated effectively at each stage from early sub-clinical lesions to late incapacitating endomyocardial fibrosis.

Adult↗
PubMed1999

Serial echocardiographic and clinical evaluation of valvular regurgitation before, during, and after treatment with fenfluramine or dexfenfluramine and mazindol or phentermine.

OBJECTIVE: The prevalence of cardiac valvular regurgitation demonstrated by echocardiography in patients who took appetite-suppressant medication for weight loss has been assessed at 5%-30%. We studied 86 patients who had echocardiograms before treatment with appetite suppressants to determine the incidence of new cases and to evaluate the clinical implication of the echocardiographic findings. RESEARCH METHODS AND PROCEDURES: We studied 69 men [Mean+/-Standard Deviation (S) age 49+/-8] and 17 women (mean+/-S age 50+/-7) who had 233 echocardiograms before, during, and after a weight-loss program that used predominantly fenfluramine (or dexfenfluramine) with mazindol (or phentermine). Mean drug exposure was 17 months. Blinded echocardiographic readings were performed to identify and grade aortic regurgitation (AR) or mitral regurgitation (MR). RESULTS: Seven of 86 patients (8%) had pre-existing regurgitation with five (6%) meeting our case definition. Thirteen (16.5%) of initially normal patients developed valvular regurgitation and were new cases. Of the new cases, 12 were grade I/IV AR and one was both grade II/III MR and II/IV AR. All 13 patients were asymptomatic, and only two aortic insufficiency murmurs could be auscultated. There was significantly greater risk for developing valvulopathy for those who took medications longer than 6 months (p = 0.03), and no new cases were observed in patients exposed for less than 8 months. No increased risk associated with age, presence of hypertension, or exposure to fenfluramine-phentermine combination was demonstrated. Although there was a higher incidence of new regurgitation in women (31% vs. 13% for men), this was not statistically significant (p = 0.093). DISCUSSION: Some patients who had normal echocardiograms at baseline developed cardiac valvular regurgitation after exposure to fenfluramine or dexfenfluramine with mazindol or phentermine. The development of valvulopathy was significantly correlated with duration of exposure. The clinical implications of echocardiographically demonstrated regurgitation are uncertain, since there were only two audible murmurs and no other clinically relevant signs or symptoms among the patients.

Aortic Valve Insufficiency↗
PubMedDate not supplied

Acardiac twin with externalized intestine adherent to placenta: unusual manifestation of omphalocele.

TRAP (twin reversed arterial perfusion) syndrome produces an acardiac twin (acardiac monster, acardius, acardiacus, chorioangiopagus parasiticus, etc.). Acardiacs result from monozygotic multiple births in which three anatomic anomalies occur: (1) a fetus' cardiac development is disturbed; (2) artery-artery anastomosis carries blood from a normal ("pump") twin to the acardiac; (3) vein-vein anastomosis carries blood from the acardiac back to the normal twin. Whether reversal of blood flow in the acardiac results from or causes cardiac dysmorphogenesis has not been resolved. Acardiac twins demonstrate a complex constellation of malformations usually thought to result from reversed blood flow; omphalocele is particularly common. We report monochorionic monoamnionic male twins in which an acardiac twin demonstrated externalized intestines adherent to the placenta. The twins were delivered from a 30-year-old primigravida mother by cesarean section without maternal complications at 33 w. The mother has no significant past medical history. The macerated acardius had a 4-cm long attenuated umbilical cord with indeterminate number of vessels. Structures rostral to the thorax were absent save for one poorly developed hand and arm. The abdomen contained loose mesenchyme and no organs. The entire intestine (21 cm) along with two testes was located in a sac on the surface of the placenta. No histopathologic anomalies of formed structures were identified aside from spatial relationships and incomplete development. The normal twin required no intensive care and is doing well. To our knowledge, this is the first report of externalized intestine, which may represent an unusual consequence of omphalocele.

Adult↗
PubMedDate not supplied

Effects of probucol on hyperlipidemic patients with cardiac allografts.

Probucol, a well-tolerated new drug with moderate hypocholesterolemic effect in the general population, was evaluated in hypercholesterolemic (greater than 300 mg/dl) cardiac transplant recipients. Nine patients received probucol, 500 mg twice daily, in a single-blind, placebo-controlled trial lasting 20 weeks. Six patients responded with cholesterol falls of -20% (mean, -13.2%), and 1 patient showed minimal change. One patient developed cardiac rejection and was excluded, and another responded paradoxically and was returned to previous therapy. In 1 patient, probucol was readministered, and a similar favorable response occurred, which has been sustained for over 6 months. For the group completing the study, low-density lipoprotein (LDL) cholesterol fell by 15.4%, accounting for the major portion of overall change in plasma cholesterol. High-density lipoprotein (HDL) cholesterol also fell (-15.6%), and the LDL/HDL ratio was unchanged. Triglycerides and very low density lipoprotein cholesterol showed variable responses with no overall change. Probucol was universally well tolerated, without adverse clinical or laboratory effects. In conclusion, probucol may effect a moderate hypocholesterolemic response in hyperlipidemic recipients of cardiac transplantation, despite long-term maintenance therapy with corticosteroids. However, efficacy should be individually documented. The long-term effect of probucol on the natural history of coronary artery disease in these patients remains to be determined, particularly in view of its effects on HDL cholesterol.

Adult↗
PubMed1991

Glycoprotein synthesis and secretion. Expression of fibronectin and its cell surface receptors.

Fibronectin (FN) is an extracellular matrix protein that acts as a substrate for cell migration and adhesion during development. Cells adhere to FN through integral membrane proteins that are members of the integrin family of adhesion molecules. The interaction between cells and FN is important in a number of biologic processes, including gastrulation, hematopoietic differentiation, neural crest cell migration, cardiac development, branching morphogenesis in lung, wound healing, tumorigenesis, and metastasis. Expression of FN and its receptors is controlled by a number of hormones and growth factors as well as by tissue-specific factors. Here, the molecular aspects of how expression of these genes is controlled are reviewed, with particular emphasis on promoter regulator elements that modulate expression.

Fibronectins↗
PubMed1979

Influence of 19-nor-deoxycorticosterone on blood pressure, saline consumption, and serum electrolytes, corticosterone, and renin activity.

Young, unilaterally nephrectomized, female Sprague-Dawley rats were given daily sc injections of 19-nor-deoxycorticosterone acetate (19-nor-DOCA) in oil at a dosage of 100 micrograms/day for 21 days and twice that amount for a further 11 days. One group drank distilled water and another drank 1% NaCl solution. Comparable control groups received oil injections. Another group received DOCA at the same steroid dosage and drank saline. Both 19-nor-DOCA-treated groups rapidly became hypertensive and developed cardiac hypertrophy, as did those given DOCA and saline. Saline consumption was greater in rats receiving 19-nor-DOCA, than in those given DOCA. Rats injected with 19-nor-DOCA and given water to drink showed enhanced growth and developed thymus enlargement and displayed hypokalemia and a reduction in both serum renin activity and corticosterone concentration. Plasma sodium concentration was not affected by any form of treatment. Clearly, 19-nor-DOCA is a potent mineralocorticoid and hypertensogenic agent. Since the parent steroid is known to be present abundantly in the urine of rats with regenerating adrenal glands, although circulating amounts have not yet been ascertained in that circumstance, it may be etiologically involved in adrenal regeneration hypertension, which such rats are prone to develop.

Animals↗
PubMed2006

Trichloroethylene exposure during cardiac valvuloseptal morphogenesis alters cushion formation and cardiac hemodynamics in the avian embryo.

It is controversial whether trichloroethylene (TCE) is a cardiac teratogen. We exposed chick embryos to 0, 0.4, 8, or 400 ppb TCE/egg during the period of cardiac valvuloseptal morphogenesis (2-3.3 days' incubation) . Embryo survival, valvuloseptal cellularity, and cardiac hemodynamics were evaluated at times thereafter. TCE at 8 and 400 ppb/egg reduced embryo survival to day 6.25 incubation by 40-50%. At day 4.25, increased proliferation and hypercellularity were observed within the atrioventricular and outflow tract primordia after 8 and 400 ppb TCE. Doppler ultrasound revealed that the dorsal aortic and atrioventricular blood flows were reduced by 23% and 30%, respectively, after exposure to 8 ppb TCE. Equimolar trichloroacetic acid (TCA) was more potent than TCE with respect to increasing mortality and causing valvuloseptal hypercellularity. These results independently confirm that TCE disrupts cardiac development of the chick embryo and identifies valvuloseptal development as a period of sensitivity. The hypercellular valvuloseptal profile is consistent with valvuloseptal heart defects associated with TCE exposure. This is the first report that TCA is a cardioteratogen for the chick and the first report that TCE exposure depresses cardiac function. Valvuloseptal hypercellularity may narrow the cardiac orifices, which reduces blood flow through the heart, thereby compromising cardiac output and contributing to increased mortality. The altered valvuloseptal formation and reduced hemodynamics seen here are consistent with such an outcome. Notably, these effects were observed at a TCE exposure (8 ppb) that is only slightly higher than the U.S. Environmental Protection Agency maximum containment level for drinking water (5 ppb) .

Animals↗
PubMed1998

Clinical cardiac magnetic resonance spectroscopy--present state and future directions.

MR spectroscopy opens a window to the non-invasive evaluation of various aspects of cardiac metabolism. Experimentally, the method has extensively been used since 1970's. 31P-MR allows the registration of cardiac high-energy phosphate metabolism to non-invasively estimate the energetic state of the heart: ATP, phosphocreatine, inorganic phosphate, monophosphate esters and intracellular pH can all be quantitated. In conjunction with extracellular shift reagents such as [DyTTHA]3- or [TmDOTP]5-, 23Na- and 39K-MR allow the measurement of intra- and extra-cellular cation pools. 1H-MR spectroscopy allows the detection of a large number of metabolites such as, e.g. creatine, lactate, or carnitine. Human cardiac spectrocsopy has so far been confined to the 31P nucleus. Localization techniques (DRESS, ISIS, 3D-CSI etc.) are required to confine the acquired signal to the heart region. Relative quantification is straightforward (phosphocreatine/ATP ratio), absolute quantification (mM) is under development. Cardiac 31P-MR spectroscopy has research application in at least three clinical areas: (1) Coronary artery disease: A biochemical stress test for non-invasive ischemia detection (decrease of phosphocreatine with exercise) and viability assessment via quantification of ATP may become feasible. (2) Heart failure: The phosphocreatine/ATP ratio may provide an independent index for grading of heart failure, allow to monitor the longterm effects of different forms of drug therapy on cardiac energy metabolism in heart failure, and may also hold prognostic information on survival. (3) Valve disease: It is possible that the decrease of phosphocreatine/ATP can be used to guide the timing for the valve replacement. At the present time, no routine clinical applications can be defined for the use of human cardiac spectroscopy in patients with cardiac disease. However, the technique holds great potential for the future as a non-invasive approach to cardiac metabolism, and in coming years routine applications may become reality.

Adenosine Triphosphate↗
PubMed2001

Integrins and the myocardium.

Extracellular matrix provides a structural, chemical, and mechanical substrate that is essential in cardiac development, growth, and responses to pathophysiological signals. Transmembrane receptors termed integrins provide a dynamic interaction of environmental cues and intracellular events. Integrins orchestrate multiple functions in the intact organism including organogenesis, regulation of gene expression, cell proliferation, differentiation, migration, and death. They are expressed in all cellular components of the cardiovascular system, including the vasculature, blood, cardiac myocytes and nonmuscle cardiac cells. The focus of this review will be on the role of integrins in the myocardium. We will provide background on integrin structure and function, discuss how the expression of integrins is critical to the form and function of the developing and postnatal myocardium, and review the known data on integrins as signaling molecules in the heart. Finally, we will offer insights to the future research directions into this important family of extracellular matrix receptors in the myocardium.

Animals↗
PubMed2003

Molecular pathways in myocardial development: a stem cell perspective.

The heart has long been considered to adapt to increased work or pathology through the cellular growth process of hypertrophy. However, recent evidence for the existence of endogenous stem cells and regenerative capacity in the adult heart has given new impetus to the quest for cell therapies for heart failure, which remains the number one killer in Western cultures. The molecular cues driving cardiac development are now being explored in detail and will come into sharp focus as regimes for stem cell differentiation and efforts to augment endogenous regeneration are trialed. This review briefly outlines the current state of knowledge on the molecular basis of the four modalities of myogenesis that have been identified in the developing vertebrate heart. Stem cell-mediated myogenic repair in the heart represents a fifth modality, and an exciting frontier with basic and practical implications that remain to be explored.

Animals↗
PubMed1998

Vertebrate homologs of tinman and bagpipe: roles of the homeobox genes in cardiovascular development.

In Drosophila, dorsal mesodermal specification is regulated by the homeobox genes tinman and bagpipe. Vertebrate homologs of tinman and bagpipe have been isolated in various species. Moreover, there are at least four different genes related to tinman in the vertebrate, which indicates that this gene has been duplicated during evolution. One of the murine homologs of tinman is the cardiac homeobox gene Csx or Nkx2.5. Gene targeting of Csx/Nkx2.5 showed that this gene is required for completion of the looping morphogenesis of the heart. However, it is not essential for the specification of the heart cell lineage. Early cardiac development might therefore be regulated by other genes, which may act either independently or in concert with Csx/Nkx2.5. Possible candidates might be other members of the NK2 class of homeobox proteins like Tix/Nkx2.6, Nkx2.3, nkx2.7, or cNkx2.8. Murine Tix/Nkx2.6 mRNA has been detected in the heart and pharyngeal endoderm (this study). Xenopus XNkx2.3 and chicken cNkx2.3 are expressed in the heart as well as in pharyngeal and gut endoderm. In contrast, murine Nkx2.3 is expressed in the gut and pharyngeal arches but not the heart. In zebrafish and chicken, two new NK-2 class homeoproteins, nkx2.7 and cNkx2.8, have been identified. Zebrafish nkx2.7 is expressed in both, the heart and pharyngeal endoderm. In the chicken, cNkx2.8 is expressed in the heart primordia and the primitive heart tube and becomes undetectable after looping. No murine homologs of nkx2.7 or cNkx2.8 have been found so far. The overlapping expression pattern of NK2 class homeobox genes in the heart and the pharynx may suggest a common origin of these two organs. In the Drosophila genome, the tinman gene is linked to another NK family gene named bagpipe. A murine homolog of bagpipe, Bax/Nkx3.1, is expressed in somites, blood vessels, and the male reproductive system during embryogenesis (this study), suggesting that this gene's function may be relevant for the development of these organs. A bagpipe homolog in Xenopus, Xbap, is expressed in the gut masculature and a region of the facial cartilage during development. In this paper, we discuss molecular mechanisms of cardiovascular development with particular emphasis on roles of transcription factors.

Amino Acid Sequence↗
PubMed1994

Cardiac adaptations to chronic exercise in mice.

Transgenic mice can be created to serve as models of human cardiac disease. Despite the technology available to manipulate the cardiovascular system of the mouse, there is relatively little information available concerning the normal physiology of the mouse heart. Therefore, we have characterized the response of the adult mouse to chronic physical conditioning by swimming. Adult female C57/B16 mice were conditioned by swimming up to 90 min twice daily for 4 wk, resulting in a 10% increase in heart weight and a 16% increase in heart weight-to-body weight ratios compared with sedentary controls. The heart rate response to a submaximal work load decreased > 20% with this conditioning program. Succinate dehydrogenase activity increased markedly in the soleus muscles of the conditioned animals, from 28 +/- 3 to 44 +/- 3 nmol.mg-1.min-1. In contrast to these changes, which also characterize the exercise model in the rat, no increase in cardiac tissue norepinephrine content or in cardiac myosin or myofibrillar adenosinetriphosphatase (ATPase) activities was observed, and no change in the V1 predominant myosin isoform or alpha-myosin heavy chain mRNA profiles was seen in the hearts of the swimmers. This study establishes that mice are able to develop cardiac hypertrophy in response to chronic conditioning which is not associated with changes in the ATPase activities of cardiac muscle. These data should be of use to investigators using murine models to define the molecular basis of adaptive cardiac hypertrophy in vivo.

Adaptation, Physiological↗
PubMed2006

Cardiomyocyte-specific deletion of the coxsackievirus and adenovirus receptor results in hyperplasia of the embryonic left ventricle and abnormalities of sinuatrial valves.

The coxsackievirus and adenovirus receptor (CAR), which mediates infection by the viruses most commonly associated with myocarditis, is a transmembrane component of specialized intercellular junctions, including the myocardial intercalated disc; it is known to mediate cell-cell recognition, but its natural function is poorly understood. We used conditional gene targeting to investigate the possible functions of CAR during embryonic development, generating mice with both germline and tissue-specific defects in CAR expression. Homozygous germline deletion of CAR exon 2 or cardiomyocyte-specific gene deletion at embryonic day 10 (E10) mediated by Cre recombinase expressed under the control of the cardiac troponin T promoter resulted in death by E12.5; embryos showed marked cardiac abnormalities by E10.5, with hyperplasia of the left ventricular myocardium, distention of the cardinal veins, and abnormalities of sinuatrial valves. Within the hyperplastic left ventricle, increased numbers of proliferating cells were evident; persistent expression of N-myc in the hyperplastic myocardium and attenuated expression of the trabecular markers atrial natriuretic factor and bone morphogenic protein 10 indicated that proliferating cardiomyocytes had failed to differentiate and form normal trabeculae. In electron micrographs, individual CAR-deficient cardiomyocytes within the left ventricle appeared normal, but intercellular junctions were ill-formed or absent, consistent with the known function of CAR as a junctional molecule; myofibrils were also poorly organized. When cardiomyocyte-specific deletion occurred somewhat later (by E11, mediated by Cre under control of the alpha-myosin heavy chain promoter), animals survived to adulthood and did not have evident cardiac abnormalities. These results indicate that during a specific temporal window, CAR expression on cardiomyocytes is essential for normal cardiac development. In addition, the results suggest that CAR-mediated intercellular contacts may regulate proliferation and differentiation of cardiomyocytes within the embryonic left ventricular wall.

Animals↗
PubMed2000

Out-of-hospital succinylcholine-assisted endotracheal intubation by paramedics.

STUDY OBJECTIVE: To describe the effectiveness and safety of succinylcholine administration by paramedics to out-of-hospital patients requiring endotracheal intubation. METHODS: A consecutive case series was collected by retrospective review of patient care records from a large, private ambulance agency serving an urban and rural county of 600,000 residents over a 40-month period. All patients for whom endotracheal intubation was facilitated by succinylcholine use were identified. Data were systematically collected on demographics, paramedic diagnosis, intubation attempts, and complications. RESULTS: Succinylcholine was used in 150 patients with a mean age (+/-SD) of 50+/-23 years. Paramedic diagnosis was coma in 43% (64/150; 95% confidence interval [CI] 35% to 51%), trauma in 26% (39/150; 95% CI 19% to 33%), and respiratory failure in 31% (47/150; 95% CI 23% to 39%). No patient was in cardiac arrest at the time of succinylcholine use. The intubation success rate was 92% (138/150; 95% CI 88% to 96%), with success achieved on the first attempt in 82% of patients (123/150; 95% CI 76% to 88%). Four patients who received succinylcholine developed cardiac arrest, and 3 others had symptomatic bradycardia. CONCLUSION: The use of succinylcholine by paramedics to assist intubation appears to aid in intubation of patients who are not in cardiac arrest. However, significant cardiac complications can occur.

Adolescent↗
PubMed2000

Cardiac toxicity after anthracycline chemotherapy in childhood.

The clinical use of anthracyclines, a family of chemotherapeutic agents with efficacy against many solid tumors and leukemias is limited by unique cumulative dose-limiting cardiotoxicity. Overt heart failure occurs in 4.5% to 7% of patients treated with anthracyclines and the incidence of cardiac function abnormalities increases with the time. Anthracycline-induced congestive heart failure is usually due to permanent changes in the myocardium, changes most consistent with the contractile failure of cardiomyopathy. Although the causes of anthracycline-induced cardiotoxicity are probably many, a large body of evidence points to free-radical-mediated myocyte damage. The risk of developing cardiac heart failure is modified by the presence of certain risk factors that reduce cardiac tolerance to anthracyclines. Age and female gender seem to have an important role in the anthracycline cardiotoxicity. This cardiotoxicity can be divided, on the base of when it started, into acute, subacute and progressive late, chronic form. Various invasive and non-invasive methods have been used to measure the extent of cardiac damage done. Depending on the sensitivity of the method employed, the proportion of hearts found to be damaged has varied widely. Attempts to ameliorate anthracycline cardiotoxicity have been directed toward: 1. decreasing myocardial concentrations of anthracyclines and their metabolites, 2. developing less cardiotoxic analogous, and 3. concurrently administering cardioprotectants to attenuate the effects of anthracyclines on the heart. Much progress has been made in terms of monitoring of clinical and subclinical anthracycline cardiotoxicity, finding alternative schedules, introducing special carriers of anthracyclines and using cardioprotecting agents. It is hoped that with all these effects and with results of ongoing and future trials, we will be able to reduce further or even eliminate anthracycline cardiotoxicity.

Age Factors↗
PubMed1999

Does the subepicardial mesenchyme contribute myocardioblasts to the myocardium of the chick embryo heart? A quail-chick chimera study tracing the fate of the epicardial primordium.

Morris (J. Anat., 1976;121:47-64) proposed that the subepicardial mesenchyme might represent a continuing source of myocardioblasts during embryonic and fetal development. Recent studies have shown that the epicardium and subepicardial mesenchyme, and the coronary vasculature are all derived from a region of the pericardial wall, called the proepicardial serosa. In avian embryos, the cells from the proepicardial serosa colonize the heart via a secondary tissue bridge formed by attachment of proepicardial villi to the heart. In the present study, Morris's hypothesis was tested by tracing the fate of the proepicardial serosa. This was achieved by constructing quail-chick chimeras. The proepicardial serosa was transplanted from HH16/17 quail embryos to HH16/17 chick embryos (ED3). A new transplantation technique facilitated an orthotopic attachment of the quail proepicardial villi to the chicken heart, and prevented the attachment of the chicken proepicardial villi to the heart. The fate of the grafted quail cells was traced in chimeras from ED4 to ED18 with immunohistochemistry, using quail-specific antibodies (QCPN, QH-1). From ED4 onward, the transplant was connected to the dorsal heart wall via its proepicardial villi. Starting from the point of attachment of the quail proepicardial villi to the heart, the originally naked myocardium became almost completely covered by quail-derived epicardium, and quail mesenchymal cells populated the subepicardial, myocardial, and subendocardial layers including the av-endocardial cushions. Quail cells formed the endothelial and smooth muscles cells of the coronary vessels, and the perivascular and intramyocardial fibroblasts. Quail myocardial cells were never found in the subepicardial, myocardial, and subendocardial layers. This suggests that the subepicardial mesenchyme normally does not contribute a substantial number of myocardioblasts to the developing avian heart. The new transplantation technique presented facilitates the production of chimeric hearts in which the derivatives of the proepicardial serosa are almost completely of donor origin. This technique might be useful for future studies analyzing the role of certain genes in cardiac development by the creation of somatic transgenics.

Animals↗
PubMed2002

Reversible cardiac arrest after polidocanol sclerotherapy of peripheral venous malformation.

BACKGROUND: Polidocanol sclerotherapy is a well-established therapeutic modality for the treatment of venous malformations. Systemic complications are extremely rare. OBJECTIVE: To report a case of cardiac complication after polidocanol injection of peripheral venous malformation. METHODS: A case report and a review of the English language literature using a published MEDLINE search strategy. RESULTS: A patient undergoing polidocanol sclerotherapy for a symptomatic venous malformation of the right inferior limb developed cardiac arrest shortly after injection of the sclerosing agent which was promptly reversed. CONCLUSION: Systemic complications following sclerotherapy may occur even when the sclerosant is injected in peripheral veins or venous malformations. Clinicians should be alerted to the possibility of uncommon but life-threatening adverse effects.

Arteriovenous Malformations↗
PubMed2002

Cardiotoxicity following different doses and schedules of 5-fluorouracil administration for malignancy -- a survey of 427 patients.

BACKGROUND: Although cardiotoxicity associated with 5-Fluorouracil (5-FU) administration is infrequent, there are case reports of acute coronary syndromes. We report on patients undergoing 5-FU chemotherapy who developed cardiac symptoms during its administration. MATERIAL/METHODS: In patients receiving 5-FU who experienced cardiac-related symptoms, ECG and serum cardiac enzyme determination were performed. If cardiotoxicity was detected, 5-FU infusion was interrupted, and the patients received sublingual nitrates and cardiac monitoring, while patients with more than 2-fold elevated enzyme levels were monitored in a coronary care unit for at least 72 hours. In cases of acute myocardial infarction, 5-FU was terminated. RESULTS: Of 427 patients entering the study, 17 (4%) developed clinical symptoms and ECG abnormalities indicating 5-FU cardiotoxicity. Patients with continuous infusion (c.i.) of 5-FU had a higher incidence of cardiotoxicity (12/197, 6%) than the remaining (5/235, 2.1%) (p=0.067), but more toxicity was encountered in patients with c.i. of 5-FU+LV for 24 hours for 5 days than in patients with the same regimen of 5-FU without LV (p<0.027) or patients with short 5-FU+LV administration (p=0.024). Seven of the 17 patients with 5-FU cardiotoxicity had an acute myocardial infarction, 4 developed ischemic changes, while 4 more patients had ECG abnormalities consistent with coronary vasospasm, of whom one subsequently died. CONCLUSIONS: The present study supports the toxic effect of 5-FU on myocardium, which is largely schedule-dependent. Considerable vigilance is required when using this drug, and its toxic effect on the coronary endothelium and myocardium merit further investigation.

Aged↗