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PubMed1989

Heart and heart-lung transplantation: the Stanford experience.

As of October 1989, over 560 patients with end-stage heart disease have received heart transplants at Stanford. In addition, 70 patients have received heart-lung transplants (H-L Tx) and 5 patients received single-lung transplants for end-stage pulmonary disease. Cyclosporine A (CsA) significantly improved survival, especially during the first posttransplant year. All patients now receive maintenance CsA, prednisone (P), and azathioprine (AZA). Fourteen-day prophylactic OKT3 significantly reduces early rejection after heart transplantation. One-year survival for cardiac transplants is 82% using CsA and 73% for our recent H-L Tx group. All 5 patients are alive after single-lung transplantation. Children with heart transplants and patients bridged to transplant with a Novacor ventricular assist system have a 1-year survival rate similar to routine heart transplant patients. Beyond the first year, heart transplant mortality continues at 5% per year. Transplant coronary artery disease (Tx CAD) accounts for 33% of the mortality, and other patients require retransplantation for Tx CAD. Cytomegalovirus contributes to the development of TX CAD and antiviral agents are being used for the early treatment of CMV infections. Cytomegalovirus is also thought to contribute to obliterative bronchiolitis (OB), the late complication that threatens H-L Tx patients. Surveillance bronchoscopy and pulmonary function tests can be used to detect early lung infection and rejection. Hopefully this will lead to improved late graft function. Future immunosuppressive efforts will be directed toward decreasing the morbidity and mortality after the first year in both heart and lung transplant patients.

Adult↗
PubMed1987

Heart and heart-lung transplantation Papworth Hospital 1979 to 1987.

The quality of life for those who survive the first 3 months after transplantation is generally good. The duration of hospital stay and the cost of transplantation per patient have been reduced during the last 3 years. Cardiologists are coming to appreciate the therapeutic potential of both heart and heart-lung transplantation and one of the chief logistic problems faced is that of increasing the provision of transplant services to match the increasing demand. Ultimately this will be donor-limited but at present in the United Kingdom the main limitation to the expansion of services is restriction of funding and resources. (The allocation for heart transplantation from the DHSS for the financial year 1987/88 is 4.3 million pounds). The broad principles of management of heart and heart-lung recipients have been established. Further improvement in medium-term results can be anticipated as a result of reducing CsA-induced nephrotoxicity and hypertension as a result of triple therapy and adjusting the components of that therapy to the individual needs of particular patients. Heart transplantation has now taken its place as an established therapy for life-threatening heart disease. Heart-lung transplantation is still going through its developmental phase with acceptable short-term results, but with much to learn in the mid- and long-term following transplantation.

Adolescent↗
PubMedDate not supplied

Extended comparison of quality of life between stable heart failure patients and heart transplant recipients.

Heart failure has been associated with poor quality of life, which can improve after heart transplantation. Long-term quality-of-life comparisons between patients with heart failure stabilized with medical therapy and heart transplant recipients have not been performed. We assessed quality of life at the time of heart transplantation evaluation and again after 41 months in 12 patients with advanced heart failure stabilized with medical therapy and in 19 patients who had gone on to undergo heart transplantation. Quality of life was measured by three questionnaires. Both groups had similar quality-of-life and clinical features during the transplantation evaluation. Over time, feelings of anxiety and depression, psychologic adaptation, and perceived functional capability improved in the transplant recipients. However, transplant recipients reported more weakness after surgery; this was the major symptom that limited activities. At follow-up 41 months later, we found no significant differences in quality-of-life changes over time between patients stabilized with medical therapy and heart transplant recipients. Overall quality of life for patients who remain stable while receiving medical therapy may not be significantly different from patients who have undergone transplantation.

Aged↗
PubMed1994

[The incidence, mechanisms and clinical factors predictive of sudden death in patients with severe heart failure evaluated in anticipation of heart transplantation].

INTRODUCTION AND OBJECTIVES: Sudden death is not uncommon in patients with severe congestive heart failure. The aim of our study was to assess the incidence, mechanisms and clinical predictors of sudden death in a large series of patients with severe congestive heart failure evaluated for heart transplantation. METHODS: With this aim we have reviewed our experience on 240 consecutive patients with severe heart failure studied in our hospital from May 1986 to June 1992. Heart failure was due to ischemic heart disease in 35% of patients and idiopathic dilated cardiomyopathy in 65%. Age was 47 +/- 12 years, left ventricular ejection fraction was 20 +/- 6%, and symptom class was IV in 88% of patients and III in 12%. RESULTS: Sixty-eight of the 240 patients (28%) died without transplantation. Death was sudden in 21 patients (31% of deaths, and 9% of all patients), due to heart failure in 41 (68%), and due to malignancy (ampuloma) in 1 (1%). Mechanism of sudden death could be identified in 12 cases: ventricular tachycardia/fibrillation in 8 and bradycardia/electromechanical dissociation in 4. On multivariate analysis (stepwise logistic regression), a lower tolerated captopril dosage (p = 0.004), a lower systolic blood pressure (p = 0.079) and a history of a ventricular tachycardia/fibrillation (p = 0.073) were independent predictors of sudden death. CONCLUSIONS: It seems possible to identify, between patients with severe heart failure, a subgroup of patients at higher risk for sudden death by means of such simple clinical parameters.

Acute Disease↗
PubMed1985

The carcinoid syndrome: comparison of 21 necropsy subjects with carcinoid heart disease to 15 necropsy subjects without carcinoid heart disease.

Carcinoid heart disease is a morphologically specific type of cardiac disorder that involves the mural and valvular endocardium on the right side of the heart. Twenty-one subjects (57 percent) (Group I) with carcinoid heart disease and 15 subjects (43 percent) (Group II) without carcinoid heart disease were studied at necropsy. The two groups were similar in mean age (54 years versus 55 years), duration of clinical illness (4.7 years versus 6.3 years), body weight (50 kg versus 52 kg), systemic blood pressure (117/77 mm Hg versus 128/77 mm Hg), blood hematocrit levels (37 percent versus 36 percent), total serum protein levels (6.0 g/dl), and serum albumin levels (2.2 g/dl versus 2.6 g/dl). The two groups were different in the frequency of the presence of precordial murmurs consistent with tricuspid regurgitation and/or pulmonic stenosis (95 percent versus 13 percent), cardiomegaly by chest radiography (38 percent versus 0), low voltage on electrocardiography (47 percent versus 0), and location of the primary site of the carcinoid tumor. Total electrocardiographic 12-lead QRS voltage was similar in each group (105 mm versus 132 mm) (10 mm = 1 mV). Of Group I subjects, 43 percent died of cardiac causes; none of the Group II subjects died of cardiac causes. Of the 21 subjects with carcinoid heart disease, seven had left-sided cardiac involvement, but in none was it of functional significance. Thus, although carcinoid heart disease frequently is the cause of death in patients with the carcinoid syndrome, the development of carcinoid heart disease is not related to the duration of symptoms of the carcinoid syndrome.

Adult↗
PubMed2000

["The memory effect" in healthy heart and transplanted heart. "Cor se ipse alit, se ipse movet, se ipse reget"].

The heart's memory, interpreted as information residue between a cardiac cycle and the subsequent one, is a very definite phenomenon (short- term memory) both in healthy subjects and in heart transplanted recipients. This "memory effect", we have observed by the autocorrelation and by the spectrum analysis of the values expressing the heartbeat acceleration variability (tachogram 24 h). The "memory effect" cannot be absolutely put down in heart transplanted recipients to interference or to the activity of the central and/or peripheral nervous system, because the heart transplanted is a denervated heart by definition. Moreover, an immediate regulating effect of hormonic factors in the short-term heartbeat regulation is not completely plausible. As already known, the heart transplanted responds to the emergency situation autonomously and autochthonously in proportion to the signals reaching it directly from the circle (vascular resistance, blood pressure, etc.). This implies the existence of functional memory that is likely to be inborn in the conduction system of the heart. Looking at the results of our research we can conclude: "cor se ipse alit, se ipse movet, se ipse reget" (it autonomously models itself to all the different modifications in the circle, it feeds itself as the organ propelling blood circulation and, if necessary, it carries on its kinetic activity autonomously).

Adult↗
PubMed1997

[Extracorporeal heart pump--a bridge to heart transplantation. First Norwegian experiences].

By February 1997, the number of heart transplantations at the National Hospital had reached 265. In our department, the first bridge to transplantation in using Thoratec artificial heart was performed in 1995. A 44 year-old patient with life-threatening heart failure was placed for one week on cardiopulmonary assist with an intra-aortic balloon pump and a veno-arterial cardiopulmonary bypass. Due to unceasing heart failure a Thoratec left ventricular assist device was implanted as a bridge to transplant. The patient was successfully transplanted two days after implantation of Thoratec. After eight months follow-up he is in New York Heart Association (NYHA) functional class I. Another patient, 17 years of age, and with dilated cardiomyopathy, went into cardiogenic shock while awaiting heart transplantation. For three days he had cardiopulmonary assist with intra-aortic balloon pump and venoarterial bypass with an oxygenator. After seven weeks on the left ventricular assist device he was transplanted. Although one episode of severe rejection occurred, be is in NYHA functional class I after four months follow-up. Our early experience is encouraging. Ventricular assist devices should be considered as a life support for patients scheduled for heart transplantation and expected to die within a very short time.

Adolescent↗
PubMed2006

Proteomic changes in hearts of kyphoscoliosis (ky) mutant mice in the absence of structural pathology: implication for the analysis of early human heart disease.

Complex molecular changes associated with early stage human heart disease are poorly understood and prevent the development of effective treatments of human cardiac disease. Relatively minor structural changes in early disease may accompany some conditions such as arrhythmias. Our objective was to determine if significant proteomic changes occur in heart tissues in the absence of structural pathology. We used a proteomic "pipeline" based on Ciphergen SELDI-TOF/MS, gel electrophoresis and MALDI-TOF/MS. The kyphoscoliosis (ky) mouse carries a mutation in a putative transglutaminase causing a primary skeletal muscle disease. The ky protein is expressed usually in skeletal and cardiac muscle but its absence from the ky heart causes no structural pathology making it a good model of "occult" heart disease. We discovered 20 statistically validated biomarkers discriminating ky from normal hearts, one cardiac troponin-I was reduced by 40% in ky hearts. A 17% deficit was confirmed subsequently by Western blot. Thus, the proteome of ky hearts was abnormal, giving support to our contention that this SELDI-based analytical approach is capable of making a significant contribution to the analysis of complex proteomic changes in early stage human heart disease.

Animals↗
PubMed1999

The role of cell adhesion molecules in Drosophila heart morphogenesis: faint sausage, shotgun/DE-cadherin, and laminin A are required for discrete stages in heart development.

Heart development in the Drosophila embryo starts with the specification of cardiac precursors from the dorsal edge of the mesoderm through signaling from the epidermis. Cardioblasts then become aligned in a single row of cells that migrate dorsally. After contacting their contralateral counterparts, cardioblasts undergo a cytoskeletal rearrangement and form a lumen. Its simple architecture and cellular composition makes the heart a good system to study mesodermal patterning, intergerm layer signaling, and the function of cell adhesion molecules (CAMs) during morphogenesis. In this paper we focus on three adhesion molecules, faint sausage (fas), shotgun/DE-cadherin (shg/DE-Cad), and laminin A (lam A), that are essential for heart development. fas encodes an Ig-like CAM and is required for the correct number of cardioblasts to become specified, as well as proper alignment of cardioblasts. shg/DE-Cad is expressed and required at a later stage than fas; in embryos lacking this gene, cardioblasts are specified normally and become aligned, but do not form a lumen. Additionally, cardioblasts of shg mutant embryos show a redistribution of phosphotyrosine as well as a loss of Armadillo from the membrane, indicating defects in cell polarity. The shg phenotype could be phenocopied by applying EGTA or cytochalasin D, supporting the view that Ca2+-dependent adhesion and the actin cytoskeleton are instrumental for heart lumen formation. As opposed to cell-cell adhesion, cell-substrate adhesion mechanisms are not required for heart morphogenesis, but only for maintenance of the differentiated heart. Embryos lacking the lam A gene initially developed a normal heart, but showed twists and breaks of cardioblasts at late embryonic stages. We discuss our findings in light of recent results that elucidate the function of different adhesion systems in vertebrate heart development.

Animals↗
PubMed1998

Inducible nitric oxide synthase (iNOS) in the human heart: expression and localization in congestive heart failure.

The inducible nitric oxide (NO) synthase (iNOS or NOS2) generates a prolonged release of large amounts of NO which may be cytotoxic and/or inhibit myocyte contractility. It has been suggested that this mechanism specifically contributes to heart failure caused by dilated cardiomyopathy (DCM). To test this hypothesis we compared the myocardial amount and localization of iNOS in myocardial biopsies from patients with heart failure caused by either DCM or ischemic heart disease (IHD). During heart transplantation, myocardial biopsies collected from the diseased heart after explantation were frozen in liquid nitrogen. Twenty-two patients in NYHA class III-IV were included (DCM: n = 8; IHD: n = 14). In each biopsy, iNOS expression was assessed using reverse transcription polymerase chain reaction (RT-PCR), and visualized by immunohistochemistry. iNOS was detected in all biopsies. Intriguingly, the amount of iNOS mRNA (shown as iNOS cDNA normalized to GADPH cDNA) did not differ significantly between the two groups (DCM 30 +/- 7; IHD 20 +/- 6, mean +/- S.E.M., P > 0.05). Similarly, no inter-group differences in the amount of iNOS protein (Western) were observed. iNOS was invariably located to vascular endothelial and smooth muscle cells. In addition, an iNOS reaction in relation to the myocyte membrane was found in 4 of the 22 patients. These four patients (two from each group) had significantly (P < 0.05) higher iNOS/GADPH ratios (54 +/- 20) than patients without myocyte membrane iNOS reaction (17 +/- 15). In conclusion, iNOS is expressed in the myocardium of all patients with heart failure caused by either DCM or IHD. iNOS is located primarily and invariably in the endothelium and vascular smooth muscle cells of the myocardial vasculature and its expression appears to be associated with the condition of heart failure per se rather than related to the heart failure etiology.

Adult↗
PubMed1991

Actin bundles on the right side in the caudal part of the heart tube play a role in dextro-looping in the embryonic chick heart.

The role of actin bundles on the heart looping of chick embryos was examined by using cytochalasin B, which binds to the barbed end of actin filaments and inhibits association of the subunits. It was applied to embryos cultured according to New's method. Looping did not occur when cytochalasin B was applied diffusely in the medium. Further, we disorganized actin bundles in a limited part of the heart tube to examine the role of actin bundles in each part in asymmetry formation. A small crystal of cytochalasin B was applied to the caudal part of the heart tube on either the left or right side. The disorganization of actin bundles on the left side resulted in the right-bending of the heart, an initial sign of dextro-looping (normal pattern), and right side disorganization resulted in left-bending. We suggest that actin bundles on the right side of the caudal part of a heart tube generate tension and cause dextro-looping. Embryos whose hearts bent to the right rotated their heads to the right, and embryos with left-bent-hearts rotated their heads to the left. The rotation of the heart tube may therefore decide in which direction the body axis rotates.

Actins↗
PubMed1985

Effects of diacetyl monoxime (DAM) on slow and fast action potentials of young and old embryonic chick hearts and rabbit hearts.

The effects of the negative inotropic agent, diacetyl monoxime (DAM), were studied on cardiac action potentials in young (3 day old) and old (13-18 day old) embryonic chick hearts and in rabbit papillary muscles. DAM (5-10 mM) decreased the action potential (AP) amplitude, the maximum rate of rise (Vmax), and AP duration of slow and fast APs in both young and old embryonic chick hearts. Concomitantly with these changes, the spontaneous beating rate was increased in young hearts. At 20 mM DAM, the maximum diastolic potential (MDP) was decreased. In fast APs of old embryonic chick hearts, the most prominent effect of DAM was a shortening of AP duration, the effects on AP amplitude, Vmax, and resting potential being less. In rabbit papillary muscles, DAM had little effect on the slow AP parameters except for shortening of AP duration. The onset of the DAM effects was rapid, the peak effect being attained by 5 min in all preparations. Reversal of the effects of DAM upon washout were fast, complete recovery being attained within 10 min. We conclude that DAM suppressed the slow Na+ current present in young chick embryonic hearts. The effects of DAM, up to 10 mM, on Vmax of the fast Na+-dependent APs in old embryonic chick hearts was less, and there was no effect on rabbit hearts. DAM suppressed the slow Ca2+-dependent APs in old embryonic chick hearts but not in rabbit papillary muscles, suggesting that the effect of DAM on the Ca2+ slow channels depends on the species.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMed2004

Effects of diabetes mellitus and ischemic heart disease on the progression from asymptomatic left ventricular dysfunction to symptomatic heart failure: a retrospective analysis from the Studies of Left Ventricular Dysfunction (SOLVD) Prevention trial.

BACKGROUND: Emerging data suggest that diabetes mellitus is a risk factor for the progression of established heart failure only in those patients with ischemic cardiomyopathy. Whether diabetes mellitus is a risk factor for the progression from asymptomatic left ventricular systolic dysfunction to symptomatic heart failure in patients with left ventricular dysfunction of an ischemic cause is not known. METHODS: We performed a retrospective analysis of 2821 patients with asymptomatic left ventricular systolic dysfunction from the Studies of Left Ventricular Dysfunction (SOLVD) Prevention trial. We used adjusted survival analysis to examine the effects of ischemic heart disease and diabetes mellitus on 3 prespecified study end points: (1) development of heart failure (HF) symptoms, (2) HF hospitalization, and (3) death or development of symptoms. RESULTS: There is a statistically significant interaction between the cause of left ventricular systolic dysfunction and diabetes mellitus on the risk of development of heart failure symptoms (P = .020). Patients with ischemic cardiomyopathy and diabetes had an increased risk of progression to symptomatic heart failure (HR = 1.56, P < .001), hospitalization for heart failure (HR = 2.16, P < .001), and death or development of symptoms (HR = 1.50, P < .001), compared with patients with ischemic cardiomyopathy without diabetes. In contrast, diabetes was not associated with an increased risk of reaching these end points in patients with nonischemic cardiomyopathy. CONCLUSIONS: Diabetes mellitus is a risk factor for the progression from asymptomatic left ventricular systolic dysfunction to symptomatic heart failure, but this risk appears to be confined to those patients with ischemic cardiomyopathy.

Analysis of Variance↗
PubMed2006

Hospital cost effect of a heart failure disease management program: the Specialized Primary and Networked Care in Heart Failure (SPAN-CHF) trial.

BACKGROUND: Determine the effect on hospitalization cost of a heart failure disease management (HFDM) program delivered within a diverse provider network as demonstrated in the SPAN-CHF randomized controlled trial. METHODS: The SPAN-CHF trial was a prospective randomized assessment of the effectiveness of HFDM delivered for 90 days across a diverse provider network in a heterogeneous population of 200 patients. Baseline clinical and demographic data were obtained on each patient, mortality was monitored, and hospitalizations were tracked for 90 days. Cost estimates for each hospitalization were based on a subsample of patients seen at Tufts-New England Medical Center for whom hospitalization costs were calculated. Heart failure disease management program costs were estimated using a programmatic budget model. Hospital utilization and cost data were combined to estimate medical costs for intervention and control groups. RESULTS: Heart failure disease management had a favorable effect on heart failure hospitalization, which was partially offset by noncardiac hospitalizations. The relative odds of at least one all-cause hospitalization during the intervention period trended less for the intervention group compared with the control group (0.76 [95% CI 0.38-1.51]). The point estimate of the differential hospitalization cost between control and intervention groups was a reduction in cost of $375 per patient. The net effect including the costs of the program was an increase of $488 per patient for the intervention group compared with the control group. The program would have been cost saving if HFDM costs had been 24% lower. CONCLUSION: The HFDM intervention, administered over 90 days to patients hospitalized for heart failure, succeeded in reducing the rate of heart failure hospitalizations, although this effect was partially offset by an increase in non-heart failure hospitalizations. The resulting modest reduction in all-cause hospitalization costs was exceeded by the cost of the intervention. Thus, although the reduction in heart failure may be interpreted as an improvement in health status, it could not be considered cost saving.

Cardiac Output, Low↗
PubMed2005

Rationale and design of a randomized trial to assess the effects of beta-blocker in diastolic heart failure; Japanese Diastolic Heart Failure Study (J-DHF).

BACKGROUND: Heart failure consists of two phenotypes: systolic heart failure and diastolic heart failure (DHF). A growing body of evidence demonstrated benefits of beta-blocker, angiotensin-converting enzyme inhibitor, and angiotensin II receptor blocker in systolic heart failure; however, evidence leading to therapeutic strategy of DHF is lacking. METHODS AND RESULTS: The Japanese Diastolic Heart Failure Study (J-DHF) is a multicenter, prospective, randomized trial designed to assess effects of beta-blocker in patients with DHF. A total of 800 patients (400 patients in each group) will be enrolled. The primary outcome is a composite of cardiovascular death and unplanned admission to hospital for congestive heart failure. Other outcomes include all-cause mortality, worsening of the symptoms of heart failure, or a need for modification of the treatment for heart failure. Serial assessment of echocardiographic and neurohumoral parameters and cost analysis of the treatment regimen will be conducted. The follow-up period is a minimum of 2 years. CONCLUSION: This study will provide important evidences for the treatment of DHF.

Adrenergic beta-Antagonists↗
PubMed2005

Decreased recipient survival following orthotopic heart transplantation with use of hearts from donors with projectile brain injury.

BACKGROUND: Fatal gunshot injury to the brain can cause significant alterations in the neuroendocrine state and myocardial dysfunction. Therefore heart allografts from these donors may result in graft failure following orthotopic heart transplantation (OHTx). We evaluated whether receiving a heart from a donor who died from fatal gunshot wound to the brain independently affected the outcome of transplantation. METHODS: A retrospective review of 113 consecutive patients undergoing OHTx at a university hospital from 1996 to 2002 was performed. Group 1 received hearts from donors with fatal gun shot brain injury (n = 17), and Group 2 received hearts from donors who died from other causes (n = 96). RESULTS: Recipient age, gender, United Network for Organ Sharing (UNOS) status, indication for transplantation, and other co-morbid conditions were similar in both groups. Young male donors pre-dominated in Group 1, but other donor characteristics were not significantly different. The incidence of Grade 3A rejection was higher in Group 1 than Group 2 (35% vs 6.3%, p = 0.003), as was the incidence of post-operative infection (35% vs 7.2%, p = 0.004). Actuarial survival at 1 and 5 years was significantly lower in Group 1 than in Group 2 (81% and 74% vs 97% and 94%, respectively, p = 0.005). Multivariate logistic regression analysis also demonstrated that fatal gunshot brain injury, as cause of donor death, was a risk factor for recipient mortality (p = 0.01). CONCLUSION: Receiving a heart from a donor with fatal gunshot brain injury is a significant risk factor for recipient mortality following OHTx. Cautious use of heart allograft from these donors, especially in low-risk recipients, may lead to improved outcome following heart transplantation.

Adult↗
PubMed2006

Prognostic value of plasma N-terminal pro-brain natriuretic peptide in children with congenital heart defects and open-heart surgery.

OBJECTIVE: To assess whether preoperative and postoperative plasma levels of N-terminal pro-brain natriuretic peptide (NT-proBNP) predict postoperative outcome of open-heart surgery in children. STUDY DESIGN: A prospective observational study was conducted with 40 children with congenital heart defects who were undergoing elective open-heart surgery. Plasma levels of NT-proBNP, troponin T, lactate, C-reactive protein, and total neutrophil cell counts were measured before, during, and 1 and 3 hours after the end of cardiopulmonary bypass grafting (CPB). Outcomes were assessed by means of the kind, dosage, and duration of inotropic drug use during the postoperative period, lactate concentrations, and the duration of mechanical ventilation. RESULTS: Preoperative levels of NT-proBNP were significantly increased irrespective of the type of congenital heart defect and the age of the patient. Preoperative NT-proBNP levels were higher in patients receiving prolonged postoperative inotropic drug therapy (r = 0.56, P = .0003). By means of multivariate analysis with the duration of inotropic therapy as the dependent variable, a significant impact of preoperative NT-proBNP levels, the presence of a cyanotic heart defect, the risk adjustment for congenital heart surgery score, duration of CPB time, and postoperative lactate levels were demonstrated (R squared = 76.8%, P <.0001). CONCLUSION: Preoperative NT-proBNP levels were associated with complicated postoperative outcome in children who underwent low-risk open-heart surgery. This marker may therefore be a useful tool in risk stratification of patients with congenital heart defects.

Biomarkers↗
PubMed1987

Heart rate variation and movement incidence in growth-retarded fetuses: the significance of antenatal late heart rate decelerations.

In 37 intrauterine growth-retarded fetuses, combined 1-hour recordings of fetal heart rate and body movements were made within 24 hours of elective cesarean section. Fetal body movements were recorded simultaneously by use of real-time ultrasound. The study group was divided into two subgroups, according to the presence (n = 29) or absence (n = 8) of antepartum late heart rate decelerations. Correlations were made with umbilical blood gas values obtained immediately after cesarean section. Baseline heart rate variation was reduced below the normal range in 88% of the intrauterine growth-retarded fetuses with decelerations but in only 37% of the group without decelerations. A reduction in fetal heart rate accelerations and body movements and an increase in mean heart rate also were observed only in the group with decelerations. Late heart rate decelerations were associated with low PO2 values in both umbilical artery and vein. It is concluded that in intrauterine growth-retarded fetuses reduced heart rate variation and movement incidence correlate with the presence of late heart rate decelerations before birth and with hypoxemia at birth.

Cesarean Section↗