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PubMed2006

Critical pathways in heart function: bis(2-chloroethoxy)methane-induced heart gene transcript change in F344 rats.

Gene transcript changes after exposure to the heart toxin, bis(2-chloroethoxy)methane (CEM), were analyzed to elucidate mechanisms in cardiotoxicity and recovery. CEM was administered to 5-week-old male F344/N rats at 0, 200, 400, or 600 mg/kg by dermal exposure, 5 days per week, for a total of 12 doses by study day 16. Heart toxicity occurred after 2 days of dosing in all 3 regions of the heart (atrium, ventricle, interventricular septum) and was characterized by myofiber vacuolation, necrosis, mononuclear-cell infiltration, and atrial thrombosis. Ultrastructural analysis revealed that the primary site of damage was the mitochondrion. By day 5, even though dosing was continued, the toxic lesions in the heart began to resolve, and by study day 16, the heart appeared histologically normal. RNA was extracted from whole hearts after 2 or 5 days of CEM dosing. After a screen for transcript change by microarray analysis, dose-response trends for selected transcripts were analyzed by qRT-PCR. The selected transcripts code for proteins involved in energy production, control of calcium levels, and maintenance of heart function. The down-regulation of ATP subunit transcripts (Atp5j, ATP5k), which reside in the mitochondrial membranes, indicated a decrease in energy supply at day 2 and day 5. This was accompanied by down-regulation of transcripts involved in high-energy consumption processes such as membrane transport and ion channel transcripts (e.g., abc1a, kcnj12). The up-regulation of transcripts encoding for temperature regulation and calcium binding proteins (ucp1 and calb3) only at the 2 low exposure levels, suggest that these adaptive processes cannot occur in association with severe cardiotoxicity as seen in hearts at the high exposure level. Transcript expression changes occurred within 2 days of CEM exposure, and were dose-and time-dependent. The heart transcript changes suggest that CEM cardiotoxicity activates protective processes associated energy conservation and maintenance of heart function.

Animals↗
PubMed1999

Heart failure due to ischaemic heart disease: epidemiology, pathophysiology and progression.

Ischaemic heart disease is the most common underlying cause of heart failure in industrialised countries. Its manifestations are protean with myocardial infarction being only one important facet. The prognosis of patients with heart failure due to ischaemic heart disease also appears to be worse than that associated with many other aetiologies. The presence of ischaemic heart disease may influence both the efficacy and choice of treatment. Agents such as digoxin and amlodipine appear less effective in patients with ischaemic heart disease while ACE inhibitors and beta-blockers appear as or more effective in patients with ischaemic heart disease. Many have expressed an opinion about how coronary disease should be managed in the patient with heart failure supported by little or no evidence. There are major theoretical and practical concerns about the use of anti-coagulant, anti-platelet and statin therapy in patients with heart failure as well as major theoretical benefits. Only randomised controlled trials will resolve these issues. The same may be said of revascularisation. Fortunately trials addressing all these areas are under way. This should put the management of coronary disease in patients with heart failure on a firm evidence-based footing.

Animals↗
PubMed1998

Pregnancy after heart or heart-lung transplantation: a series of 10 pregnancies.

OBJECTIVE: To evaluate pregnancy after heart or heart-lung transplantation in France. DESIGN: A questionnaire survey of all French centres performing heart and heart-lung transplants provided an exhaustive registry on pregnancy after transplantation. METHODS: A questionnaire was sent to 36 centres. Anonymous reports on transplantation and subsequent pregnancies between 1984 and 1996 were analysed. RESULTS: Of 1290 heart and 120 heart-lung transplantation performed during the study period, 10 pregnancies (seven after heart transplantation and three after heart-lung transplantation) were reported in nine women who were delivered of 11 infants. High blood pressure complicated nine pregnancies and severe pre-eclampsia occurred in two. One woman developed Kaposi sarcoma of the cervix. Delivery at 35 weeks gestation (27-39) was by caesarean section in 50% cases. Mean birthweight was 1990 g (700-2880g) and 50% of the infants had a birthweight < tenth centile. One infant developed cardiomyopathy as a condition inherited from her mother, and congenital hepatitis B was diagnosed in another. CONCLUSIONS: Pregnancy after heart and heart-lung transplantation is feasible and can be successful, but this should be planned when cardiac and respiratory functions are stable. Adequate obstetrical and genetic counselling should be provided.

Adult↗
PubMed1996

Contribution to heart rate variability by mechanoelectric feedback. Stretch of the sinoatrial node reduces heart rate variability.

BACKGROUND: Heart rate variability is an important prognostic indicator for sudden death. An increased risk of sudden death and arrhythmia is associated with reduced heart rate variability in heart failure. In heart failure, there is also dilatation of the atria, which raises the prospect that there could be some physiological basis to possibly link heart rate variability with atrial dilatation. We therefore investigated whether sustained atrial stretch could modulate heart rate variability directly. METHODS AND RESULTS: Pigs were anesthetized and their hearts exposed. A specially built device stretched the sinoatrial node before and after vagal section and then after administration of propranolol. Stretch of the sinoatrial node decreases heart rate variability in the following ways: The standard deviation of the beat-to-beat interval decreases (4.2 to 2.6 ms; P = .004), and the high-frequency components are reduced (control, 6.5 +/- 2.2 ms2, during stretch, 1.4 +/- 0.3 ms2, P = .003). After section of both vagi, the high-frequency components are reduced by stretch of the sinoatrial node (2.8 +/- 0.9 ms2 for control versus 1.2 +/- 0.3 ms2 during stretch; P = .05). Similarly, after both vagal section and beta-blockade, stretch of the sinoatrial node reduces the high-frequency components (10.6 +/- 3.5 ms2 for control verses 3.0 +/- 1.5 ms2 during stretch; P = .01). CONCLUSIONS: We conclude that stretch of the sinoatrial node reduces high-frequency heart rate variability. This may account in part for the reduced heart rate variability seen in clinical conditions in which the right atrium is dilated, such as congestive cardiac failure.

Adrenergic beta-Antagonists↗
PubMed1983

Energy levels at systole vs. diastole in normal hamster hearts vs. myopathic hamster hearts.

The following studies were carried out to examine energy metabolites and cardiac performance of the failing heart (hereditary cardiomyopathy) of the Syrian hamster (strain UM-X7.1) perfused either by normal or stress conditions, and to determine whether cyclical changes in energy-related metabolites occurred in the glucose-perfused hearts of both normal and heart failure animals. Hamster hearts from 250-day-old animals with moderate heart failure were removed and perfused either as nonworking hearts (Langendorff method, an afterload pressure of 90 mm Hg and 2.5 mM calcium in the perfusate) or as working hearts with stress conditions [an afterload of 110 mm Hg, high calcium concentrations in the perfusate (3.5 mM), and 10(-8) M isoproterenol]. Mechanical parameters (developed pressure and max dP/dt) and measurements of oxygen consumption indicated that both contractility and oxygen consumption had fallen 50% in myopathic hearts, compared with those of normal hamsters perfused with either of the two conditions. By means of a specially designed stimulator-triggered freeze clamp, hearts were terminated at systole and diastole, and tissue content of ATP, ADP, AMP, adenosine, phosphocreatine, creatine, pyruvate, lactate, and inorganic phosphate were analyzed. A 50% reduction in cardiac performance of the cardiomyopathic hamster hearts was associated with a corresponding reduction in systolic ATP, adenosine, and phosphocreatine values, while inorganic phosphate and lactate increased. With glucose as the sole substrate, the high energy phosphates, ATP and phosphocreatine, reached maximum values during diastole and minimum values during systole.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine↗
PubMed2001

UT-A urea transporter protein in heart: increased abundance during uremia, hypertension, and heart failure.

Urea transporters have been cloned from kidney medulla (UT-A) and erythrocytes (UT-B). We determined whether UT-A proteins could be detected in heart and whether their abundance was altered by uremia or hypertension or in human heart failure. In normal rat heart, bands were detected at 56, 51, and 39 kDa. In uremic rats, the abundance of the 56-kDa protein increased 1.9-fold compared with pair-fed, sham-operated rats, whereas the 51- and 39-kDa proteins were unchanged. We also detected UT-A2 mRNA in hearts from control and uremic rats. Because uremia is accompanied by hypertension, the effects of hypertension per se were studied in uninephrectomized deoxycorticosterone acetate salt-treated rats, where the abundance of the 56-kDa protein increased 2-fold versus controls, and in angiotensin II-infused rats, where the abundance of the 56 kDa protein increased 1.8-fold versus controls. The 51- and 39-kDa proteins were unchanged in both hypertensive models. In human left ventricle myocardium, UT-A proteins were detected at 97, 56, and 51 kDa. In failing left ventricle (taken at transplant, New York Heart Association class IV), the abundance of the 56-kDa protein increased 1.4-fold, and the 51-kDa protein increased 4.3-fold versus nonfailing left ventricle (donor hearts). We conclude that (1) multiple UT-A proteins are detected in rat and human heart; (2) the 56-kDa protein is upregulated in rat heart in uremia or models of hypertension; and (3) the rat results can be extended to human heart, where 56- and 51-kDa proteins are increased during heart failure.

Adult↗
PubMed1978

Information variables in voluntary control and classical conditioning of heart rate: field dependence and heart-rate perception.

Two experiments focused on two information variables relevant to changes in heart rate, field dependence and the ability to perceive one's own heart rate. In Exp. I, 14 field-independent and 17 field-dependent subjects completed a heart-rate perception and a voluntary heart-rate control task. The anticipated superiority in heart-rate control by field-independent subjects was detected although no evidence was found for a relationship between the amount of biofeedback available in the situation and voluntary control of the cardiovascular system. Exp. II involved 9 field-independent and 8 field-dependent subjects in a classical conditioning paradigm involving shock sensitivity. In contrast with Exp. I, in this phase of the study heart-rate increases were correlated with the ability of the subject to discriminate heart beats, especially for the field-independent group. It was concluded that field dependence and heart-rate perception are related to classically conditioned heart-rate increase for some subjects and further that field dependence may be a potent variable operating in those situations involving the voluntary control of heart rate without exteroceptive feedback.

Biofeedback, Psychology↗
PubMed1999

Acute and chronic effects of a hypocaloric diet on 24-hour blood pressure, heart rate and heart-rate variability in mildly-to-moderately obese patients with essential hypertension.

We examined the acute and chronic effects of a nutritionally balanced, moderately hypocaloric diet on 24-hour ambulatory blood pressure, heart rate and heart-rate variability in mildly-to-moderately obese patients with essential hypertension. We enrolled 16 obese patients with essential hypertension [age: 51-76 years, body mass index (BMI): 26-32 kg/m2]. For the initial week, a standard diet of 2,000 kcal/day was given, followed by a 3-week of a hypocaloric diet of 850 kcal/day. In the last period of the standard diet and in the first and the last periods of the hypocaloric diet, each subject's 24-hour ambulatory blood pressure, heart rate and R-R intervals of the electrocardiogram were recorded, and electrolytes and catecholamines in 24-hour urine samples were also measured. A power spectral analysis of the heart-rate variability was performed over a 24-hour period based on the autoregressive method. The subjects lost 3.7+/-0.3 kg (mean +/- s.e.m.) of body weight during the 3-week hypocaloric diet period. The 24-hour blood pressure did not differ between the last period of the standard diet and the first period of the hypocaloric diet; however, it showed a significant reduction after 3 weeks of the hypocaloric diet. The decrease in the 24-hour blood pressure during the study period was 10.5+/-1.5 mm Hg systole and 4.3+/-1.8 mm Hg diastole. In contrast, the 24-hour heart rate was significantly reduced in the first period of the hypocaloric diet, although the body weight and blood pressure did not change, and the rate was maintained even in the last period of the hypocaloric diet. The decrease in the 24-hour heart rate during the study period was 2.8+/-0.9 beats per minute. The hypocaloric diet did not change any autonomic indices obtained from a power spectral analysis of the heart-rate variability. In conclusion, different responses to a hypocaloric diet were observed between the blood pressure and the heart rate in obese hypertensive patients. The changes in power spectral parameters of the heart-rate variability were less apparent than those found with the blood pressure or the heart rate.

Blood Pressure↗
PubMed2002

Smooth muscle cells transplantation is better than heart cells transplantation for improvement of heart function in dilated cardiomyopathy.

Muscle cell transplantation may delay or prevent cardiac dilation in dilated cardiomyopathy. The present study was designed to compare the effects of the heart function of smooth muscle cell (SMCs) auto-transplantation and heart cell (CMs) allo-transplantation in dilated cardiomyopathic hamsters, and to determine which cells are better for cell transplantation. CMs and SMCs were isolated from BIO 53.58 hamsters, and cultured for transplantation. CMs, SMCs (4 X 10(6) cells each) or culture medium were transplanted into 17 weeks old BIO 53.58 hamsters to achieve CM transplantation (CMTx), SMC transplantation (SMCTx), and controls (Con) (N=10 each). Cyclosporine (5 mg/Kg) was administered subcutaneously to CMTx. Healthy hamsters (sham, N=6) were used to compare heart functions. Four weeks after transplantation, heart function was evaluated in all groups using a Langendorff perfusion apparatus. Histology demonstrated severe focal myocardial necrosis in the dilated cardiomyopathic hearts. CMTx and SMCTx formed huge muscle tissue in the dilated myocardium. Sham, SMCTx, and CMTx had a better heart function than Con (p < 0.01), and SMCTx had a better peak systolic pressure (p < 0.05) and developed pressure (p < 0.05) than CMTx at any balloon volume. However, sham and SMCTx were not statistically different. SMCTx and CMTx formed muscle tissue and produced better heart function in the cardiomyopathic hearts, and SMCTx showed better systolic and developed pressures than CMTx, even though they were similar in other functions. Significantly, SMCTx had heart functions, which were similar to those of healthy hamster's hearts.

Animals↗
PubMed2005

Immunological aspects of the statins' function in patients with heart failure: a report from the Annual Conference of ESC - Heart Failure 2005.

The annual meeting of the Heart Failure Association of ESC in Lisbon, in June 2005, was exceptionally successful. There were many very interesting presentations and workshops with the unique title: Statins in heart failure- Cholesterol-lowering is not the only goal. Heart failure (HF) is a progressive disease with coronary artery disease (CAD) as the most often underlying etiology. Treatment to prevent progression of heart failure has been targeted to reverse the consequences of HF and to a less extent the cause - the atherosclerotic plaque itself. On the average 50% of patients with heart failure are treated with lipid intervention. Lipid-lowering treatment with statins clearly reduces morbidity and mortality of patients with documented CAD. Since the prevalent etiology of heart failure is CAD, its prevention may reduce heart failure progression. However, recent studies suggest that pleiotropic effects of statins are more important than the influence related to their cholesterol lowering mechanism. Furthermore it is suggested that low levels of circulating lipoproteins and cholesterol may be independent predictors of impaired outcome in patients with heart failure. There are some possible explanations for this finding. High levels of cholesterol can be beneficial to heart failure patients; cholesterol-rich serum lipoproteins are able to modulate inflammatory immune function because they bind and detoxify bacterial lipopolysaccharide, a very strong stimulator of the release of proinflammatory cytokines that promote heart failure progression and death. So current recommendations strongly emphasize that the aim of treatment of HF is not to lower cholesterol.

Disease Progression↗
PubMed1994

The effects of left heart assist on right ventricular muscle mechanics and ventricular coupling in the injured heart.

So that we could better characterize the effects of left heart assist on right ventricular myocardial muscle mechanics and ventricular mechanical coupling in the injured heart, nine dogs underwent 30 minutes of global cardiac ischemia supported by cardiopulmonary bypass followed by randomly varied levels of left heart assist at 0, 1.0, and 2.0 L/min (0, 37 +/- 4, and 74 +/- 7 ml/kg per minute). A centrifugal pump with left ventricle-to-aorta bypass was used with the intent to cause left ventricular volume unloading but without complete left ventricular pressure unloading. Right ventricular regional free wall and septal-free wall dimensions were measured by a sonomicrometer and right ventricular pressure by a micromanometer. Pressure and dimension data were acquired over a range of preloads produced by transient vena caval occlusion and at steady state at an initial control point and after ischemia at each level of left heart assist. Right ventricular regional early diastolic function was assessed by percent segmental relaxation during the first third of diastole, end-diastolic compliance by the end-diastolic pressure-dimension relationship, systolic contractile performance by the slope (Mw) and dimension axis intercept (Lw) of the linear preload recruitable stroke work relationship, and right ventricular isovolumic relaxation by the pressure decay time constant. Ischemia reduced Mw of both the free wall (38.3 +/- 16.1 to 16.4 +/- 4.2 erg.cm-3 x 10(3), p < 0.01) and septal free wall (30.2 +/- 12.7 to 13.4 +/- 4.9 erg.cm-3 x 10(3), p < 0.01) and shifted Lw rightward (1.3 +/- 0.3 to 1.4 +/- 0.3 mm, p < 0.01, and 2.8 +/- 0.8 to 3.0 +/- 0.9 mm, p < 0.01), which confirmed myocardial ischemic injury. There were no effects of left heart assist on free wall or septal-free wall systolic contractile performance assessed by Mw and Lw or on early diastolic relaxation assessed by percent segmental relaxation during the first third of diastole in either right ventricular region (all p = not significant). There were also no observed characteristic alterations of free wall or septal-free wall end-diastolic pressure-dimension relationships with left heart assist. The pressure decay time constant decreased with increasing levels of left heart assist (51 +/- 14, 49 +/- 16, and 43 +/- 11 msec, p < 0.05), which indicated an improvement in right ventricular isovolumic relaxation attributable to left heart assist. These data demonstrate that mechanical ventricular interactive effects during left heart assist are beneficial, but limited to isovolumic relaxation in the injured heart.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed2001

Brain death-related energetic failure of the donor heart becomes apparent only during storage and reperfusion: an ex vivo phosphorus-31 magnetic resonance spectroscopy study on the feline heart.

BACKGROUND AND OBJECTIVE: Recently, we have shown, by using localized in vivo phosphorus-31 magnetic resonance spectroscopy (31P MRS) of the anterior left ventricular wall, that brain death (BD) is not associated with reduced myocardial energy status. In this study, we applied ex vivo 31P MRS of the entire heart to study the effects of BD on the energy status of the feline donor heart following explantation. METHODS: We used cats (6 BD and 6 controls [C]) in a 26-hour protocol. After 2 hours of preparation, we induced BD by filling an intracranial balloon at t = 0 hour. At t = 6 hours, the hearts were arrested with St. Thomas' Hospital cardioplegic solution, explanted, and stored in the same solution at 4 degrees C in a 4.7 Tesla magnet for 17 hours. Subsequently, the hearts were reperfused in the Langendorff mode at 38 degrees C for 1 hour. The first 5-minute 31P MRS spectrum was obtained 1 hour after crossclamping the aorta; we obtained subsequent spectra every hour during storage and every 5 minutes during reperfusion. At the end, the hearts were dried and weighed. Phosphocreatine (PCr), gamma-adenosine triphosphate (gamma-ATP), inorganic phosphate (Pi), and phosphomonoesters (PME), were expressed per g dry heart weight. The intracellular pH (pH(i)) and the PCr/ATP ratio were calculated. RESULTS: During storage, we identified a significant but similar decrease of pH(i), PCr/ATP ratio, and PCr in both groups. During reperfusion, pH(i) and PCr/ATP ratio recovered similarly in both groups, whereas the recovery of PCr in the BD group was significantly lower (p < 0.05). The Pi and PME increased in both groups during storage but to a lesser extent in the BD group (p < 0.05). This difference disappeared during reperfusion. The gamma-ATP was already significantly lower in the BD group at the onset of storage, and this remained so throughout storage and reperfusion (p < 0.05 vs C). Contractile capacity was lost in all hearts, except for 1 heart in the BD group. CONCLUSION: Brain death-related failure of the energetic integrity of the feline donor heart becomes apparent only when using 31P MRS during ischemic preservation and subsequent reperfusion.

Animals↗
PubMed1995

Spectral analysis of systolic blood pressure and heart rate after heart transplantation in children.

1. The aim of the study was to examine the short-term variability in blood pressure and heart rate in 19 children who had received heart transplants and in eight normal control children. 2. Blood pressure was determined by a finger arterial pressure device. We examined the power spectra for heart rate and systolic blood pressure in the supine and tilted positions. In addition, we studied the acute changes in blood pressure and heart rate during active standing. 3. In the transplanted children we could distinguish two groups (groups A and B) in whom heart rate variability differed, although in both it was greatly reduced compared with controls (group C). In group A there were no significant fluctuations in the mid-frequency range for heart rate. The gain of the relationship between systolic blood pressure and heart rate was very low and there were virtually no heart rate changes associated with passive tilting. 4. By contrast, in group B transplant patients the heart rate variability, as assessed by standard deviation, was about half that of normal controls. The power spectra attenuation was greater in the high-frequency than in the mid-frequency bands. On passive tilting the latter became enhanced, but not the high-frequency variability. On active standing the tachycardic response was about half that of controls. The findings suggest some reinnervation involving cardiac sympathetic fibres to a greater degree than the fast-responding vagal fibres. 5. In both groups A and B the drop in systolic blood pressure observed early in active standing was about 4-6 times as great as in controls.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Pressure↗
PubMed1996

Decreased heart rate variability in patients with congestive heart failure and chronotropic incompetence.

UNLABELLED: Heart rate variability was studied in 41 patients (aged 48 +/- 12 years) with congestive heart failure secondary to idiopathic dilated cardiomyopathy. All patients underwent a treadmill exercise test and 24-hour Holter ECG monitoring. Chronotropic incompetence was defined as the failure to achieve > or = 80% of the predicted maximal heart rate response given by 220--age (years) at peak exercise. Spectral heart rate variability was analyzed from 24-hour Holter ECGs and was expressed as total (0.01-1.00 Hz), low (0.04-0.15 Hz), and high (0.15-0.40 Hz) frequency components. The standard deviation of all normal RR intervals (SDNN) was also computed. Chronotropic incompetence was observed in ten patients. Peak oxygen consumption was significantly lower in patients with chronotropic incompetence compared with those without chronotropic incompetence. The total (5.11 +/- 1.26 ln [ms2] vs 6.41 +/- 0.92 ln [ms2]; P = 0.009) and low (3.38 +/- 1.65 ln [ms2] vs 5.45 +/- 1.34 ln [ms2]; P = 0.003), but not the high (3.42 +/- 1.04 ln [ms2] vs 4.00 +/- 1.12 ln [ms2]; P = 0.249) frequency components of heart rate variability were significantly lower in patients with chronotropic incompetence, although there was no significant difference in mean heart rate (88 +/- 20 beats/min vs 86 +/- 15 beats/min; P = 0.831) or left ventricular ejection fraction (22% +/- 10% vs 24% +/- 10%; P = 0.619). SDNN was also significantly lower in patients with chronotropic incompetence compared with those without chronotropic incompetence (64 +/- 34 ms vs 102 +/- 37 ms; P = 0.030). CONCLUSIONS: The observation that heart rate variability is significantly decreased in patients with congestive heart failure who have chronotropic incompetence suggests that chronotropic incompetence may relate to an abnormal autonomic influence on the heart in these patients.

Autonomic Nervous System↗
PubMed2001

[The neurovegetative system in heart failure and heart transplantation].

Increased sympathetic activity and plasma levels of norepinephrine, parasympathetic withdrawal and impaired baroreflex gain have been reported in patients with chronic heart failure (CHF). Since excessive neurohormonal activation is implicated in the progression of heart failure, it is crucial to measure and quantify it in clinical practice. Some techniques that may be suitable for this purpose such as catecholamine plasma level assessment or direct recording of the neural efferent activity to the peripheral muscles, require expertise and are very unattractive in terms of cost-effectiveness. On the contrary, the measures that test the reflex or tonic responses of the sinus node activity have been extensively used in both experimental and clinical studies. However, consensus regarding their true relevance in the clinical scenario has not yet been reached. Heart rate variability is one of the easiest techniques available for physicians but the identification of the RR intervals in CHF is often very difficult owing to the presence of rhythm disorders or of sino-atrial or atrioventricular blocks and the analytical softwares included in the commercially available Holter systems are not reliable enough. Similarly, for all methods currently employed in clinical practice, the assessment of baroreflex sensitivity in CHF has some limitations or is not applicable for all patients. In this article, the main clinical methods used to assess the autonomic nervous system in CHF are reviewed focusing on the clinical applicability of the obtained parameters. It is underlined that, using these techniques, many investigators have obtained important results in the pathophysiological comprehension of the disease, but to date their use in the clinical setting is very modest. Indeed, before the measurement of the autonomic nervous system can be applied to clinical practice and used to guide therapy, more precise insights into the link between the autonomic indexes and sympathetic or parasympathetic activity and between them and mortality are needed. Moreover, no standardization has been established for the various commercial systems and the development of their software has not been guided by any research committee. For many other techniques there are no commercially available devices and the software has been developed in the physiological laboratories as prototypes. These limitations will be overcome if the researchers succeed in convincing the companies about the importance and the clinical applicability of the evaluation of the autonomic nervous system. With regard to cardiac transplantation, as the donor heart is completely denervated, it constitutes an important physiological model for the study of autonomic activity. The more interesting research field has been the assessment of a possible post-transplant reinnervation both at the experimental and clinical levels. It has been shown that in animal models reinnervation occurs within the first year of heart transplantation. Several authors have demonstrated a time-dependent restoration of myocardial norepinephrine content as well as an increase in the heart rate and myocardial contractility in response to neural sympathetic stimulation. Parasympathetic efferent reinnervation has also been demonstrated in a canine transplanted model within 12 months of surgery. Despite evidence in favor of both sympathetic and parasympathetic reinnervation in animals, the problem of whether such reinnervation also occurs in humans is still debated, especially as far as parasympathetic reinnervation is concerned. The presence, in humans, of sympathetic reinnervation has been documented by different methods. However, there are significant differences regarding the degree of regeneration and the frequency of occurrence. It has also been assumed that the regeneration of sympathetic fibers takes place slowly over time. In contrast, regrowth of parasympathetic nerve fibers in patients after heart transplantation has not been unequivocally confirmed. Although various investigators have used the same method, their results differ and are indeed often contradictory. Recently it has been suggested that the type of surgery may have a major influence on neural and particularly parasympathetic regeneration. If the patients undergo heart transplantation by bicaval techniques the nerves are resected and they are more prone to regenerate towards the donor heart. This is not true if the traditional technique is employed.

Autonomic Nervous System↗
PubMed1989

Regulation of mitochondrial matrix pH and adenosine 5'-triphosphatase activity during ischemia in slow heart-rate hearts. Role of Pi/H+ symport.

During ischemia in so-called slow heart-rate hearts, there is a marked inhibition of the mitochondrial ATPase mediated by inhibitor protein binding to the enzyme (Rouslin, W., and Pullman, M. E. (1987) J. Mol. Cell. Cardiol. 19, 661-668). This ischemia-induced ATPase inhibition is triggered by a drop in mitochondrial matrix pH (Rouslin, W. (1987) J. Biol. Chem. 262, 3472-3476) which occurs as a result of the cell acidification which develops rapidly during the ischemic process. One effect of the ATPase inhibition is a marked slowing of the net rate of tissue ATP hydrolysis and, thus, a prolongation of cell viability during ischemia. In the present study, we demonstrate that matrix acidification in intact mitochondria from slow heart-rate hearts appears to be mediated by the Pi transporter. Pi/H+ symport appears to be the primary process which mediates matrix acidification and thus ATPase inhibition in intact slow heart-rate heart mitochondria made acidotic in vitro and, presumably, also in mitochondria in situ during the ischemic process. In contrast, intact mitochondria from a so-called fast heart-rate species, which exhibited only a low level of ischemia-induced ATPase inhibition in situ (Rouslin, W. (1987) Am. J. Physiol. 252, H622-H627), failed to exhibit a Pi- and pH-dependent mitochondrial ATPase inhibition mechanism in vitro. The Pi-dependent mitochondrial ATPase inhibition mechanism reported here for slow heart-rate hearts is consistent with a role for Pi as a coordinating signal promoting the conservation of cell ATP during myocardial ischemia.

Adenosine Triphosphatases↗
PubMed1982

Changes in indications for heart transplantation. An additional argument for the preservation of the recipient's own heart.

The 1 year survival rate after heart transplantation since 1967 from +/-30% to +/-70%, and the 5 year survival rate is now +/-50%. This improvement has brought renewed interest in this procedure, now done in about twenty centers in eight countries, and increased confidence has widened the indication to patients who are less than terminally ill, to restore quality of life. This trend is illustrated by the Cape Town series, which can be divided into two parts: 10 patients treated by orthotopic heart transplantation (OHT), from 1967 to 1973, and 40 patients treated by heterotopic heart transplantation (HHT), from 1974 to 1981. The HHT group was younger (mean 37 +/- 10 years versus 51 +/- 9 years, p less than 0.001), had been ill for a shorter length of time (mean 3.6 +/- 0.7 years versus 6.6 +/- 1.4 years, p less than 0.091), and were in a lower New York Heart Association (NYHA) class (mean 3.45 +/- 0.11 versus 3.9 +/- 1.0, p less than 0.006). The improved survival is linked to patient selection, progress in management, and switch to HHT, but not to progress in matching between donor and recipient. Since there is no means to predict tolerance of the donor heart, HHT limits the risks from unforseeable mismatch. The recipient's heart is a built-in assist device, maintaining life when the donor heart fails acutely at operation or during acute [three cases] or chronic [two cases] rejection. Had these patients undergone OHT they would have died. Comparing the 10 oldest HHT patients with the OHT series, no difference in pretransplant parameters was found. However, survival of HHT recipients was longer during the critical post-HHT period: at 3 months, p less than 0.011; at 6 months, p less than 0.05. Larger series will separate the effects of progress in management from the intrinsic advantages of HHT. Retaining the recipient's heart is logical and has brought few complications. Survival rate of 40 HHT patients was 73% at 6, 65% at 12, and 51% at 36 months; 85% of survivors are in NYHA Class I. In patients in less than desperate condition, but who refuse to remain cripples, HHT eliminates the growing ethical problem of removing a recipient's heart that may still support the patient.

Adolescent↗
PubMedDate not supplied

Anatomic constraints for a total artificial heart in orthotopic heart transplant recipients.

The anatomic constraints and design parameters for a heart prosthesis have not yet been defined in heart transplant recipients (i.e., the population most eligible for total artificial heart implantation). The parameters regarding anatomic constraints were measured in 26 consecutive patients undergoing orthotopic heart transplantation (median body surface area 1.9 m2) after cardiectomy. A full-sized contour model of the cylindric total artificial heart (diameter 97 mm; width 81 mm) was inserted into the pericardial cavity to decide the pump configuration and to verify its fit. The dimensions of this model were based on the miniature electromechanical total artificial heart that is currently under development. Fit was found to be adequate in most of the cases with no identifiable compression of adjacent vascular structures. The median intraoperative measurements that define pericardial constraints for a heart prosthesis were pericardial length (130 mm), width (160 mm), and depth (140 mm). We also took measurements from the excised hearts, which should provide a useful reference for other prosthetic devices. The current dimensions of our implantable total artificial heart were found acceptable for orthotopic implantation. Length of the pericardium and cardiothoracic ratio were identified as variables related to adequacy of fit.

Adult↗