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PubMed1992

The University of Ottawa Heart Institute Cardiac Transplant Program: the first 100 transplants. A pathologic study of the explanted hearts.

Since 1984, 122 orthotopic heart transplants have been performed at the University of Ottawa Heart Institute. Of the 114 adult patients, 100 (87.8%) were males and 14 (12.2%) females, with mean ages of 45.8 and 47.9 yr, respectively. The hearts of these adults were pathologically diagnosed as chronic ischemic heart disease (CIHD) in 55 (48.2%), acute ischemic heart disease (AIHD) in 17 (14.9%), dilated cardiomyopathy (DC) in 30 (26.3%), valvular heart disease in five (4.4%), congenital heart disease in three (2.6%), myocarditis in three (2.6%), and other in one (0.9%) of the cases. The adult hearts (94) among the first 100 transplants were studied morphologically, to look for differences among the three major groups with clinical "end-stage" heart failure. The mean heart weights were 435, 356, and 463 gm in the CIHD, AIHD, and DC groups, respectively, with AIHD less than CIHD or DC (p less than 0.01). The ventricular wall thicknesses were similar in CIHD and DC, but the left ventricular (LV) wall thicknesses in AIHD were more than in CIHD or DC (p less than 0.01). The ventricular diameters were greater in DC than in CIHD or AIHD (p less than 0.01) and greater in CIHD than in AIHD (p less than 0.01). The mean LV cavity volumes were 158, 94, and 200 ml in CIHD, AIHD, and DC, respectively, with DC greater than in CIHD or AIHD (p less than 0.01) and CIHD greater than in AIHD (p less than 0.01). The relative differences in AIHD compared to CIHD and DC are referrable to the shorter duration of disease in the acute ischemic group.2+ off

Acute Disease↗
PubMed1996

Normalization of total body and regional sympathetic hyperactivity in heart failure after heart transplantation.

BACKGROUND: Sympathetic nerve activity is increased in patients with severe heart failure. Whether this intense sympathoexcitation is normalized after heart transplantation, despite cyclosporine A treatment, is still unsettled. In the present study, regional sympathetic function in 12 patients with severe heart failure, awaiting heart transplantation, was compared with that in 15 heart transplant recipients and 12 healthy subjects. METHODS: Total and regional sympathetic activity in the heart and kidney were evaluated with isotope dilution, using steady-state infusion of [3H] norepinephrine. Sympathetic nerve traffic to skeletal muscle vascular bed was recorded intraneurally with microneurography. RESULTS: Total body, cardiac, and renal norepinephrine spillovers were high in the heart failure group (6792 +/- 455, 385 +/- 74, and 1554 +/- 114 pmol/min, respectively) as was muscle sympathetic nerve activity (82 +/- 5 bursts/min). Transplant recipients showed a marked reduction of total body (3200 +/- 307 pmol/min) and renal (747 +/- 169 pmol/min) norepinephrine spillovers and sympathetic nerve firing to skeletal muscle (22 +/- 6 bursts/min), none of which differed from healthy subjects. CONCLUSIONS: The augmentation of total body and regional sympathetic outflow to the kidney and skeletal muscle vascular beds, associated with a failing heart, was normalized after transplantation. Thus, sympathoexcitation in heart failure is reversible. Furthermore, because all heart transplant recipients received cyclosporine A, the findings do not support the concept that cyclosporine-induced hypertension is mediated by increased sympathetic nerve activity.

Adult↗
PubMed2001

Heart transplantation and the Batista operation for children with refractory heart failure.

Medically refractory heart failure may be present in children with cardiomyopathy (CMP) or complex congenital heart disease (CHD). In adults, the surgical management of this condition is either heart transplantation or the Batista operation. From March 1995 to January 2000, a total of 6 children, aged from 1 to 16 years, with medically refractory heart failure associated with CMP or complex CHD underwent cardiac transplantation and one of them also had the Batista operation as a bridge to transplantation. One of the 6 patients died of intractable sepsis 17 days after the operation, but the other 5 were discharged with satisfactory hemodynamics. Immunosuppressive agents, including azathioprine, cyclosporin or FK-506, were given. One patient experienced moderate acute rejection, but it was controlled by FK-506, OKT-3 and solumedrol. However, another suffered from lymphoproliferative disease 8 months after transplant, but it was controlled by intravenous immunoglubulin, alpha-interferon and acyclovir. Cardiac function during serial follow-up (range, 1 month to 5 years) revealed normal systolic and diastolic function and none received any anticongestive medications. Almost all patients received an oversized donor heart. The left ventricle (LV) mass was remodeled, initially as an decrease and later as an increase. The patient who underwent the Batista operation was discharged 1 month after the operation with an increased LV ejection fraction (from 10% to 22%). She was successfully bridged to heart transplantation 7 months after the Batista operation. The results of cardiac transplantation in growing children are satisfactory and remain the mainstay of surgical treatment for medically refractory heart failure in these patients. However, with a shortage of donor hearts, the Batista operation may be adopted as a bridge to heart transplant with a fair response.

Adolescent↗
PubMed1999

Inhibition of Na+-H+ exchanger protects diabetic and non-diabetic hearts from ischemic injury: insight into altered susceptibility of diabetic hearts to ischemic injury.

It has been previously suggested that alterations in sodium homeostasis, leading to calcium overload may play a part in the mediation of cardiac ischemic injury. It has been demonstrated that the Na+-H+ exchanger plays an important role with regard to the regulation of intracellular sodium during ischemia and reperfusion and that inhibition of the Na+-H+ exchanger during ischemia protects hearts from ischemic injury. Studies using chemically-induced diabetic animals have suggested that the cardiac Na+-H+ exchanger in the diabetic heart is impaired and is responsible for limiting the increase in sodium during ischemia. The extent to which the Na+-H+ exchanger contributes to increases in intracellular sodium during ischemia in diabetic hearts is unclear as direct measurements of exchanger activity have not been made in genetically diabetic hearts. Therefore, this paper aims to address the following issues: (a) is the Na+-H+ exchanger impaired in a genetically diabetic rat heart: (b) does this impairment result in lower [Na]i or [Ca]i during ischemia; and (c) does Na+-H+ exchanger inhibition limit injury and functional impairment in diabetic hearts during ischemia and reperfusion? These issues were examined by inhibiting the Na+-H+ exchanger with ethylisopropylamiloride (EIPA) in isolated perfused hearts from both genetically diabetic (BB/W) and non-diabetic rats. Levels of intracellular sodium, intracellular calcium, intracellular pH and high energy phosphates (using 23Na,19F, 31P NMR spectroscopies, respectively) during global ischemia and reperfusion were also measured. The impact of diabetes on Na+-H+ exchanger activity was assessed by measuring pH recovery of these hearts after an acid load. Creatine kinase release during reperfusion was used as a measure of ischemic injury. This study demonstrated that the Na+-H+ exchanger is impaired in diabetic hearts. Despite this impaired activity, inhibition of Na+-H+ exchanger protected diabetic hearts from ischemic injury and was associated with attenuation of the rise in sodium and calcium, and limitation of acidosis and preservation of ATP during ischemia. The data presented here favor the use of Na+-H+ exchanger inhibitors to protect ischemic myocardium in diabetics. Also, the data provides possible mechanisms for the altered susceptibility of diabetic hearts to ischemic injury.

Acidosis↗
PubMed1988

Parental death from heart disease and the risk of heart attack.

In the British Regional Heart Study, 7735 men aged 40-59 years were asked at initial screening whether their father or mother was alive or dead and to what cause any death had been attributed. They were followed up for the occurrence of major ischaemic heart disease events. At screening the men reported that 23% of the fathers and 43% of the mothers were alive and that 19% of the fathers and 11% of the mothers had died of heart trouble. In a sample of parental deaths, the death certificate was obtained and it was found that a son's report of a parental death from 'heart trouble' was a reliable indication that death had been certified to ischaemic heart disease. However, about half of the parental deaths certified as ischaemic heart disease were not reported as 'heart trouble' by their sons. A major ischaemic heart disease event was experienced by 336 men over an average follow-up of 6.2 years. Men who said their father had died from 'heart trouble' were at twice the risk of a major ischaemic heart disease event compared with men whose fathers were still alive and 1.5 times the risk of men who reported their father to be dead from another or unknown cause, even after accounting for age, systolic blood pressure, serum total cholesterol, cigarette smoking and serum HDL-cholesterol. For men with mother dead from heart trouble, the corresponding figures were 1.3 and 1.0.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

The role of risk factors in heart attacks occurring in men with pre-existing ischaemic heart disease.

The importance of three risk factors--serum total cholesterol, systolic blood pressure, and cigarette smoking--on the risk of new major ischaemic heart disease events in men who already have evidence of ischaemic heart disease was assessed. Data from the initial examination in a large prospective study of cardiovascular disease in middle aged men (the British Regional Heart Study) were used to separate 7710 men into three groups on the basis of a resting electrocardiogram, a standardised chest pain questionnaire, and recall of a doctor's diagnosis of angina or of a previous heart attack: (group 1) no evidence of ischaemic heart disease (75%), (group 2) evidence of ischaemic heart disease short of a definite myocardial infarction (20%), (group 3) definite myocardial infarction (6%). In the average follow up period of 7.5 years, 443 men suffered a new major event caused by ischaemic heart disease (fatal or non-fatal myocardial infarction or sudden cardiac death). Age standardised event rates were determined for each of the three groups for varying levels of the established risk factors. Cigarette smoking is strongly associated with the event rate in group 1 but in men with existing heart disease, especially group 3, differences in risk between the smoking categories were smaller. The strong relation between systolic blood pressure and event rate persisted in groups 1 and 2 but not in group 3. The positive association between serum concentration of total cholesterol and the event rate was strongest in group 1 and weaker in groups 2 and 3, though it remained highly significant. These observations, taken together with the results of previous prospective studies and intervention trials, suggest that the important association between serum total cholesterol and the risk of heart attack persists in men with pre-existing ischaemic heart disease, including myocardial infarction. Therefore, in these men the reduction of serum total cholesterol concentration may be at least as important as it is in men without evidence of ischaemic heart disease.

Adult↗
PubMed1996

Carvedilol inhibits clinical progression in patients with mild symptoms of heart failure. US Carvedilol Heart Failure Study Group.

BACKGROUND: We tested the hypothesis that carvedilol inhibits clinical progression in patients with mildly symptomatic heart failure due to left ventricular (LV) systolic dysfunction. METHODS AND RESULTS: Patients (n = 366) who had mildly symptomatic heart failure with an LV ejection fraction (LVEF) < or = 0.35, had minimal functional impairment (defined as the ability to walk 450 to 550 m on a 6-minute walk test), and were receiving optimal standard therapy, including ACE inhibitors, were randomized double-blind to carvedilol (n = 232) or placebo (n = 134) and followed up for 12 months. The primary end point was clinical progression, defined as death due to heart failure, hospitalization for heart failure, or a sustained increase in heart failure medications. Clinical progression of heart failure occurred in 21% of placebo patients and 11% of carvedilol patients, reflecting a 48% (P = .008) reduction in the primary end point of heart failure progression (relative risk, 0.52; CI, 0.32 to 0.85). This effect of carvedilol was not influenced by sex, age, race, cause of heart failure, or baseline LVEF. Carvedilol also significantly improved several secondary end points, including LVEF, heart failure score, NYHA functional class, and the physician and patient global assessments. Carvedilol reduced all-cause mortality but had no effects on the Minnesota Living With Heart Failure scale, the distance walked in 9 minutes on a self-powered treadmill, or cardiothoracic index. The drug was well tolerated. CONCLUSIONS: Carvedilol, when added to standard therapy, including an ACE inhibitor, reduces clinical progression in patients who are only mildly symptomatic with well-compensated heart failure.

Adolescent↗
PubMed2000

Management of heart failure: evidence versus practice. Does current prescribing provide optimal treatment for heart failure patients?

Heart failure is an increasingly common and costly chronic disorder, with a rising prevalence of at least 2% in populations over the age of 45 years, mortality rates that are as poor as common solid cancers, and very high health care utilisation costs. Despite increased evidence supporting a range of effective interventions, predominantly therapeutic, there remain significant degrees of physician underperformance in terms of heart failure diagnosis and management. Until the early 1990s, the management of heart failure was largely confined to the symptomatic relief of patients with well established heart failure in fluid overload. The introduction of angiotensin-converting enzyme (ACE) inhibitors provided the first treatments that beneficially altered the prognosis of patients with the most common expression of heart failure, namely established systolic dysfunction, whether symptomatic or asymptomatic. Evidence has now extended these benefits to delaying progression of heart failure and reducing hospitalisation. Much of our understanding of the pathophysiology of heart failure stems from these studies. More recent data has clarified the limited role of digoxin, the important benefits of beta-blockade and aldosterone blockers as adjuvants to ACE inhibition, and the emerging evidence on angiotensin II antagonists. There are, in contrast to these positive findings, reliable data from Europe and North America revealing significant underperformance of primary care and hospital physicians in heart failure diagnosis and management, with evidence of underuse and underdosing of evidence-based therapies. Limited qualitative data suggest the reasons for this underperformance are complex and relate to lack of access to objective testing of ventricular function and exaggerated concerns over treatment risks and side-effects. Heart failure represents a complex cluster of aetiologies and risks that are not easy to correctly identify, even in specialist settings. Since there is now powerful evidence on how heart failure can be modified and improved, explicit guidance is needed for which suspected patients should be referred, for confirmation of diagnosis and advice on appropriate treatment regimes, and for which patients can be handled mainly within primary care but with enhanced access to objective non-invasive tests to improve diagnostic reliability and to stratify patients to evidence-based therapies. Current evidence suggests that in North America and Europe today primary care physicians do underperform in their management of patients with heart failure, often owing to factors outside of their immediate control.

Adrenergic beta-Antagonists↗
PubMed1994

Cloning and expression of fibroblast growth factor receptor-1 isoforms in the mouse heart: evidence for isoform switching during heart development.

Basic (b) fibroblast growth factor (FGF) mediates various biological responses including mitogenesis and angiogenesis by binding to specific cell surface receptors of the tyrosine kinase family. The bFGF receptor-1 FGFR1) exists in short and long isoforms due to alternate RNA splicing. Minor alterations in the amino acid sequence have also led to reports of different FGFR1 isoforms in different tissues even in the same species. In the absence of any sequence for heart FGFR1 and accumulating evidence for a role of bFGF in heart growth and differentiation, we cloned FGFR1 from embryonic mouse hearts. Reverse transcriptase-polymerase chain reaction (RT-PCR) was used to generate full-length short (2259 base pairs) and long (2526 base pairs) forms of FGFR1 cDNAs which generated 86 and 102 kDa proteins, respectively, following in vitro translation. Embryonic mouse heart FGFR1 differed by seven amino acids from the reported sequence for mouse neuroepithelial FGFR1 and appeared more similar to human placental FGFR1. A single FGFR1 transcript of approximately 4.3 kb was seen in RNA isolated from embryonic as well as adult mouse hearts. There was a decrease (approximately 8.5-fold) in FGFR1 RNA levels in the adult. The majority of FGFR1 transcripts in the adult as well as embryonic heart contained exon IIIc (FGFR1-IIIc) which is associated with isoforms that display the highest affinity for bFGF. However, the relative ratio of short versus long FGFR1 RNA expression was 0.5 in the embryonic heart compared to 5.9 in the adult heart. These results indicate that: (i) structurally distinct short and long FGFR1 isoform RNAs are expressed in the embryonic and adult heart; (ii) FGFR1-IIIc is the major form of receptor expressed in the embryonic as well as adult heart; (iii) the transition from the embryo to the adult stage is associated with a decrease but not absence of FGFR1 RNA expression; and (iv) long FGFR1-isoforms are more abundant in the embryo while short FGFR1 isoforms predominate in the adult.

Amino Acid Sequence↗
PubMed1992

Heart rate and oxygen uptake response to exercise in children with low peak exercise heart rate.

Normal children achieve the same increase of oxygen uptake (VO2) in response to exercise even though resting and submaximal exercise heart rates vary greatly as a function of age, body size and physical conditioning. To determine whether the VO2 response to exercise is altered when heart rate is significantly reduced by heart disease, we compared 78 children who achieved a peak exercise heart rate of less than or equal to 150 beats/min to 201 controls of similar body size and normal peak exercise heart rates of greater than or equal to 180 beats/min. All performed incremental (16.4 Watts/min) maximal cycle exercise. Separate analysis of males and females included heart rate, power (kg-m/min, Watts/kg), VO2 (ml/min, ml/min per kg), O2 pulse (VO2/heart beat), VE (l/min) and R (VCO2/VO2) at rest and during the 1st, 4th and last minute of exercise. Patients with low peak exercise heart rates had also lower resting submaximal exercise heart rates than controls. VO2 at comparable exercise levels did not differ from controls and consequently O2 pulse was greater in the patients than controls at rest and at all levels of exercise. A consistent gender difference was only found in controls where males achieved a higher VO2 and lower heart rates at comparable levels of exercise. The data show a normal exercise VO2 despite significantly lower heart rates. These findings cannot be explained by an increased arteriovenous difference alone and suggest that the patients retained the ability to effectively modulate stroke volume.

Adolescent↗
PubMed1999

Intravenous ganciclovir prophylaxis for cytomegalovirus in heart, heart-lung, and lung transplant recipients.

Cytomegalovirus (CMV) disease has had a significant clinical impact on the heart, heart-lung and lung transplant recipients in our centre. CMV disease has been so severe with CMV antibody-negative heart-lung transplant patients receiving organs from CMV antibody-positive donors (CMV-mismatched patients) that in 1986 we adopted the policy of not transplanting CMV-positive organs into CMV-negative heart-lung or lung recipients. In December 1992, we instituted a policy of providing intravenous ganciclovir (5 mg/kg twice a day for 28 days) during the immediate postoperative period for CMV-mismatched heart recipients and CMV antibody-positive heart-lung and lung patients, who have been the patients at greatest risk of severe CMV disease in our centre. A placebo group was not employed because of ethical considerations, ganciclovir having been shown to be effective for the treatment of CMV infections among transplant patients. Compared with a historical control group of patients receiving no prophylaxis, prophylactic ganciclovir reduced the incidence of CMV infection (39 % vs 91 %, P = 0.0006) and CMV disease (17 % vs 74 %, P = 0.0004) among CMV antibody-positive heart-lung recipients. Prophylactic ganciclovir did not significantly reduce the incidence of CMV infection or disease among heart or isolated lung recipients. Ganciclovir was well tolerated, with few adverse reactions. In the case of heart-lung transplant patients, one month of intravenous prophylactic ganciclovir significantly reduced the incidence of both CMV infection and disease when compared with patients who received no prophylaxis. With the lung transplant and heart transplant patients, there were no significant differences between the prophylaxis and nonprophylaxis groups, although there was a consistent trend towards less infection and disease in the prophylaxis groups.

Adolescent↗
PubMed1998

[Heart operations for heart tumors in Germany--results of 1996 survey].

In the Federal Republic of Germany, no data existed regarding the frequency of open heart surgery for excision of cardiac neoplasms. Therefore, a standard questionnaire concerning heart tumors was sent to all 77 German heart centers performing cardiac surgery. Data from 65 of the 77 heart centers (= 84%) are finally available: 187 patients were operated upon for myxomas, only 44 upon for non-myxomatous cardiac tumors (28 of them with malignant primary or secondary lesions of the heart). In 1996, 0.32% (231/72,763) of all surgical procedures using a heart-lung machine (registered 72,763 of 87,372 total) were aimed at excision of heart tumors. Based on surgical data, the incidence of solely the primary tumors of the heart in Germany is at least 3 per million population per year (253 tumors/81.814 million inhabitants). Even if small tumors are asymptomatic and remain undetected, today, the majority of primary tumors of the heart will be revealed by echocardiography, computer tomography, and magnetic resonance imaging, and these patients are usually referred to operation. Thus, in Germany, about 0.3% of operations using a heart-lung machine were performed for cardiac tumors-among these, myxomas are clearly predominant.

Adolescent↗
PubMed1995

Heart rate variability in patients with mild to moderate heart failure: effects of neurohormonal modulation by digoxin and ibopamine. The Dutch Ibopamine Multicenter Trial (DIMT) Study Group.

OBJECTIVES: This study assessed the effects of digoxin and ibopamine on variables of heart rate variability in relation to neurohormonal activation. BACKGROUND: Analysis of heart rate variability can be used to study the autonomic dysfunction that characterizes chronic heart failure. In the Dutch Ibopamine Multicenter Trial, patients with heart failure were found to have increased neurohormonal activation with placebo therapy but not with digoxin and ibopamine therapy. METHODS: We studied 59 patients with mild to moderate heart failure (mean [+/- SEM] age 60 +/- 1 years, mean ejection fraction 0.30 +/- 0.01). Patients were randomized to double-blind treatment with digoxin (0.25 mg [n = 22]), ibopamine (100 mg three times a day [n = 19]) or placebo (n = 18); background therapy consisted of furosemide (up to 80 mg). RESULTS: After 3 months, plasma norepinephrine levels had increased with placebo, whereas they decreased with digoxin (+31 vs. -60 pg/ml, respectively, p < 0.01). With ibopamine, nonsignificant decrease was observed (-27 pg/ml, p = 0.10). All variables of heart rate variability showed a deterioration in the placebo group. With digoxin, the percent differences between successive RR intervals > 50 ms (pNN50) increased (+ 1.7 +/- 0.9%, p < 0.01), along with absolute and normalized high frequency power (+ 40 +/- 33 ms2, p < 0.05 and + 2.4 +/- 1.7%, p < 0.01, respectively). These changes were observed during daytime hours only and were most pronounced in patients with the most impaired baseline heart rate variability. With ibopamine, nonsignificant trends similar to the changes with digoxin were observed. CONCLUSIONS: In patients with early stages of heart failure, digoxin may prevent a progressive deterioration in heart rate variability, whereas ibopamine does not show statistically significant effects. The changes in heart rate variability with digoxin parallel an observed decrease in neurohormonal activation. Digoxin apparently enhances cardiac vagal tone in the setting of neuroendocrine activation.

Aldosterone↗
PubMed2005

Influence of age, gender, and serum triglycerides on heart rate in a cohort of asymptomatic individuals without heart disease.

BACKGROUND: Age, sex and blood lipids were demonstrated in epidemiological studies to influence heart rate measured on physical examination, on 12-lead electrocardiogram or with automatic devices for short-term measurements. We hypothesized that in healthy individuals, age, sex and other clinical variables may also influence heart rate measured on 24-h ambulatory electrocardiographic monitoring. METHODS: We studied 625 asymptomatic individuals with normal clinical examination, aged 15 to 83 (mean 42, standard deviation 11.9) years, 276 (44.2%) men and 349 (55.8%) women. Heart rate was evaluated on 24 h ambulatory electrocardiographic monitoring. Variables selected in univariate analysis (chi(2) and Student t tests) were further submitted to multivariate analysis with canonical correlation to assess the strength of associations between heart rate and other variables, and multiple linear regression models to generate reference curves. RESULTS: Age was the most significant influence on canonical variable of heart rate relative to other clinical and laboratory variables (0.55; p<0.01). There was an increase in the minimum heart rate and a decrease of maximum heart rate with increasing age in both genders. The increase was steeper in men and the decrease was steeper in women. Minimum heart rate increased with increasing serum triglycerides and decreased as estimated maximum oxygen consumption increased. CONCLUSIONS: There was a narrower variation of heart rate with increasing age in both genders in healthy individuals. This variation was less pronounced in women. In addition, status of body haemostasis associated with peculiar metabolic conditions expressed in serum triglycerides levels may also be associated with heart rate.

Adolescent↗
PubMed1996

Role of spectral measures of heart rate variability as markers of disease progression in patients with chronic congestive heart failure not treated with angiotensin-converting enzyme inhibitors.

Measures of heart rate variability in the frequency domain quantify autonomic activity. However, the relation of these measures to the severity of ventricular dysfunction in patients with congestive heart failure remains uncertain. We applied spectral analysis of heart rate variability to 24-hour Holter monitor recordings obtained from 20 patients with congestive heart failure who were not treated with angiotensin-converting enzyme inhibitors to determine whether significant changes in parameters of heart rate variability reflect the progression of symptoms in patients with ventricular failure. Both total and low-frequency heart rate spectral power were seen to decrease with worsening New Heart Associate (NYHA) functional class. A significant (p = 0.04) higher total power was noted in NYHA class II than in class III patients (3.0 x 10(-3) +/- 3.6 10(-4) and 2.5 x 10(-3) +/- 5.9 x 19(-4) [beats/min]2, respectively). Similarly, low-frequency heart rate spectral power was significantly (p = 0.008) higher in class II than in class III patients (1.7 x 10(-3) +/- 4.6 x 10(-4) and 1.1 x 10(-3) +/- 3.5 x 10(-4) [beats/min]2, respectively). Only the low-frequency component of the spectrum was directly correlated with left ventricular ejection fraction (LVEF) (r = 0.40) with a trend toward statistical significance (p = 0.07). Measures of heart rate variability and the changes in autonomic tone that they reflect may therefore serve as markers of the extent of disease progression in patients with congestive heart failure.

Adult↗
PubMed2001

Relation of heart rate and blood pressure turbulence following premature ventricular complexes to baroreflex sensitivity in chronic congestive heart failure.

Reduced heart rate variability (HRV) and attenuated baroreflex sensitivity (BS) after myocardial infarction and in patients with chronic congestive heart failure (CHF) are associated with poor prognosis. Recent studies have shown that a large proportion of the prognostic power from HRV measurements is localized in heart rate turbulence immediately after ventricular premature complexes. The mechanism of heart rate turbulence remains unknown. In the present study, we explore its relation to BS. In 45 patients with CHF and > or =3 ectopic beats in a 30-minute period, measurements of RR interval and continuous, noninvasive blood pressure (BP) were studied at rest. In response to an ectopic beat, average heart rate turbulence was 9.4 ms/beat (SD 6.1). Mean BP turbulence was 0.72 mm Hg/beat (SD 0.56). Using the ratio of heart rate and BP turbulence slopes to estimate BS showed good agreement (r = 0.67, p < 0.0001) with the alpha-index method (BSalpha). This relation was attributable to a marked correlation between heart rate turbulence and BSalpha (r = 0.70, p <0.0001); there was no correlation between BP turbulence and the BSalpha (r = 0.1, p = NS). Twenty-nine percent of patients had postectopic pulsus alternans, with a mean decay time of 1.4 beats (SD 0.5). The presence of pulsus alternans was associated with a significantly lower heart rate turbulence slope (6.3 [SEM 1.0] vs 10.7 [SEM 1.2] ms/beat, p = 0.03). Thus, heart rate turbulence is an effective measure of the baroreflex, correlating strongly with a standard measure. This is because it is the heart rate, rather than the BP, response to an ectopic beat that conveys the information relevant to BS measurement.

Autonomic Nervous System↗
PubMed1992

Screening for congenital heart disease with the four-chamber view of the fetal heart.

OBJECTIVE: Our objective was to determine the efficacy of the four-chamber view of the fetal heart in routine ultrasonographic examination as a screening tool for congenital heart defects. STUDY DESIGN: A prospective cohort study compared the detection rate of congenital heart defects among 5336 pregnant women screened with the ultrasonographic four-chamber view of the fetal heart from 1987 through 1989 with that among 3680 patients examined ultrasonographically without the four-chamber view during the 2 preceding years (1985 through 1986). All patients were followed until delivery or termination of pregnancy, and clinical or autopsy confirmation of prenatal findings were obtained on all cases. RESULTS: The overall incidence of congenital heart diseases was 5.2 per 1000 (47/9016). During the years 1985 through 1986 15 neonates with congenital heart diseases were identified, seven of which were prenatally diagnosed (sensitivity 43%). During the period 1987 through 1989 a four-chamber view of the fetal heart was obtained in 95% of cases; 32 cases of congenital heart disease occurred, 26 of which were diagnosed antenatally (sensitivity 81%; p = 0.01). Two false-positive diagnoses were made during the second time period, giving a specificity of 99.9%. CONCLUSION: The four-chamber view of the fetal heart is easily obtained, does not significantly increase the duration of a routine ultrasonographic examination, and has an excellent sensitivity for the identification of congenital heart diseases.

Cohort Studies↗
PubMed2001

Chronic infusion of dobutamine and nitroprusside in patients with end-stage heart failure awaiting heart transplantation: safety and clinical outcome.

BACKGROUND: in patients with severe heart failure additional therapeutic support with intravenous inotropic or vasodilator drugs is frequently employed in an attempt to obtain hemodynamic and clinical control. No data comparing the use and efficacy of chronic intravenous inotropic and vasodilator therapy in patients with advanced heart failure are available. AIMS: we evaluated, in a group of patients with advanced heart failure undergoing chronic infusion with dobutamine or nitroprusside, in addition to optimized oral therapy, (1) the safety of chronic infusion, (2) the efficacy of both drugs in managing unloading therapy and (3) clinical outcome of the two therapeutic strategies. METHODS: one hundred and thirteen patients receiving optimized oral therapy, in functional class III/IV with symptoms and signs of refractory heart failure and requiring additional pharmacological support with either intravenous dobutamine or nitroprusside were evaluated. Clinical and therapeutic management and clinical outcome of the two groups were considered. RESULTS: dobutamine was administered for 12 h/day for 20+/-23 days at a dosage of 7+/-3 microg/kg/min to 43 patients. The mean dose of nitroprusside was 0.76+/-0.99 microg/kg/min. The mean duration of use of this drug, administered as a 12-h/day infusion was 22+/-38 days. Nitroprusside infusion allowed greater doses of short-term ACE-inhibitors to be used compared to pre-infusion (ACE-inhibitor dose: 55+/-30 mg/day vs. 127+/-30 mg/day P<0.0001) and during dobutamine infusion (ACE-inhibitor dose: 85+/-47 mg/day vs. 127+/-30 mg/day P<0.002). Nitroprusside unlike dobutamine significantly improved the NYHA functional class. Of the 113 patients, 109 (97%) had a cardiac event during a mean follow-up of 337+/-264 days. Forty-four patients required hospitalization for worsening congestive heart failure, 45/113 (39%) patients died during the follow-up and 27/113 (24%) patients had a heart transplant in status one. Hospitalization, because of worsening heart failure was less frequent in the nitroprusside than in the dobutamine subgroup [29/51 (57%) vs. 19/22 (86%) P<0.02]. The overall mortality was 28% (20/70) in the nitroprusside group and 58% (25/43) in the dobutamine group (odds ratio 0.33 CI 0.16 to 0.73 P<0.006). In the group treated with nitroprusside, heart transplantation in status one was performed in 16/33 patients (48%), while in the dobutamine group this was done in 11/14 patients (78%) (odds ratio 0.25 CI 0.06-1.02 P<0.06). There was a significant reduction in the combined end-point of mortality/heart transplantation in status one in patients treated with nitroprusside compared to those treated with dobutamine (36/70 (51%) vs. 36/43 (84%) - (odds ratio 0.34 CI 0.14-0.80 P<0.01). The incidence of adverse events in the patients treated with nitroprusside was similar to that in those treated with dobutamine (20% vs. 17% P=ns). CONCLUSIONS: for patients awaiting heart transplantation chronic intermittent nitroprusside infusions are more effective and safer than dobutamine in relieving symptoms, facilitating unloading therapy management and improving survival. Whether chronic intermittent infusion of nitroprusside could represent a feasible medical strategy in out-patients with severe heart failure remains to be investigated.

Cardiac Output, Low↗