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PubMed2002

[The application of electric heart assist devices in 3 patients with end-stage heart failure as a bridge to transplantation].

Left-ventricular assist devices have already gained an international place in the treatment of end-stage heart failure. It is expected that in future they will be increasingly used as a temporary bridging following the recovery from heart failure and to a lesser extent as a bridge to heart transplantation. Three patients with end-stage heart failure, men aged 68, 57 and 49 years, received a left-ventricular assist device (LVAD) as a bridge to transplantation. The device chosen was a Heartmate Vented Electric System (ThermoCardiosystems; Woburn, Massachusetts, US). In this system a pump is implanted under the diaphragm and connected to the apex of the left ventricle and the pars ascendens aortae. The first two patients reached the time of transplantation and used the LVAD for 367 and 416 days respectively. The third patient died after the pump had been implanted, due to progressive right-ventricle failure. The first patient died shortly after the heart transplantation.

Aged↗
PubMed1989

[Echocardiography of the right heart--unknown territory. Contribution of echocardiography and Doppler echocardiography to the study of the right heart].

The aim of this study involving 700 echocardiographic examinations (echoes) was to evaluate the diagnostic impact of the method for right heart abnormalities. Among 200 two-dimensional echoes of a first series we found 23 abnormalities (11.5%): nine congenital malformations, seven pulmonary hypertensions, four cases of isolated right ventricular dilatation, two tricuspid regurgitations (TR), one right atrial myxoma. In four cases the abnormality was clinically unexpected. In a second series of 500 patients, consecutively subjected to a two-dimensional echo with pulsed-wave and continuous-wave Doppler, we found 119 regurgitations of right heart valves in 98 patients (20%): 35 TR and 24 pulmonary regurgitations (PR) secondary to pulmonary hypertension, 13 TR secondary to tricuspid valve prolapse, 16 TR and 11 PR as a part of polyvalvular disease; 10 TR and 10 PR were isolated observations. The examination technique and the echo signs of the principal abnormalities of the right heart are reviewed. In summary, we emphasize that right heart abnormalities are surprisingly frequent in routine echo investigations; therefore, complete study of all the right heart structures in every echo examination is mandatory.

Echocardiography↗
PubMed1988

[Current status of use of the artificial heart in combination with heart transplantation].

Acute and therapeutically uncontrollable cardiac insufficiency in a case of chronic heart disease with acute risk of rejection and with a record of previous transplantation or during a heart operation should be considered as an indication for implantation of an artificial heart or a ventricle-supporting system, if a donor heart is not available. Two results are expected from such an approach, restoration of adequate circulation and improvement of organ functionally providing a chance for later transplantation. Attention should be given, according to the authors' own experience, to effective surgical haemostasis. Infections have quite often proved to be incurable after implantation of an artificial heart and, consequently, provide a clear-cut contraindication to implantation.

Assisted Circulation↗
PubMed1982

Biophysics of the developing heart. III. A comparison of the left ventricular dynamics of the fetal and neonatal lamb heart.

Changes in heart rate, left ventricular dimensions, and inotropic state of chronically instrumented lambs from in utero to neonatal life are described and analyzed. Six lambs were instrumented from 5 to 23 days prior to parturition and studied prior to and after birth. Heart rate, aortic systolic and diastolic pressure, left ventricular end-diastolic and peak systolic pressure, and left ventricular minor axis end-diastolic (EDD) and end-systolic dimension (ESD) were monitored. The maximum rate of rise of left ventricular pressure (Pmax), percentage fractional shortening [(EDD - ESD divided by EDD) x 100%; %FS], and the Pmax -interval ratio (this ratio of Pmax of the postextrasystolic potentiated systole to Pmax of the previous regular systole is independent of volume) described contractility. Subsequent to birth: heart rate, aortic systolic and diastolic pressure and left ventricular dimensions increased; during spontaneous rhythm and at equal fetal and neonatal heart rates and ventricular dimensions, %FS and P max increased significantly; and P max -interval ratio changed significantly. An increase in myocardial inotropic state occurs with birth. This enhancement is in addition to the effects of the increase in heart rate and end-diastolic volume that occur with the adaptation to birth.

Adaptation, Physiological↗
PubMed1994

[Concept for therapy of heart failure in heart surgery].

Perioperative deterioration of the circulatory performance of patients undergoing heart surgery ranges from transitory impairment in cardiac output by deterioration of the compensation range of the oxygen transport system to manifest circulatory failure without previous myocardial damage and the acute decompensation of pre-existing chronic heart failure. On the basis of the current state of knowledge in this field, a concept for rational staged treatment should be based on the different myocardial beta-adrenoceptor conditions related to the type and stage of the individual underlying heart disease and on adrenoceptor subtype specific properties of positive inotropic drugs. 1. The therapy of perioperative "circulatory" insufficiency after extra-corporal circulation consists of the use of drugs to adapt the performance of the oxygen transport system to increased overall oxygen demand. Simultaneous volume loading (by CVP) and positive inotropic support with dobutamine are the best means of treating this (normally transitory) dysregulation. 2. In the case of manifest severe circulatory insufficiency (low cardiac output syndrome), sepsis or acute heart failure (e.g., following acute myocardial infarction), the use of a pulmonary artery catheter for determining perioperative cardiac output and resistance is essential. In such cases, positive inotropic therapy is based on catecholamines of medium (dobutamine) to high (adrenaline) efficacy, because it can be assumed that the beta-adrenoceptor pattern will remain normal with regular functioning and regulation of the (remaining) myocardium up to the onset of acute heart failure.(ABSTRACT TRUNCATED AT 250 WORDS)

Amrinone↗
PubMed2001

Treatment of congestive heart failure: guidelines for the primary care physician and the heart failure specialist.

During the past 10 years, the philosophy of heart failure treatment has evolved from symptom control to a combined prevention and symptom-management strategy. Recent clinical trials have proved that early detection can delay progression. Treatment of asymptomatic left ventricular dysfunction is as important as treatment of symptomatic disease. The purpose of this review is to simplify recent guidelines for pharmacological management of chronic systolic heart failure for the primary care physician and the heart failure specialist. Early recognition and prevention therapies, combined with lifestyle modification, are essential in the treatment of heart failure. Therapy with angiotensin-converting enzyme inhibitors, beta-blockers, and diuretics is now standard. Digoxin is added to improve clinical symptoms, especially in patients with atrial fibrillation. Aldosterone antagonists may be recommended in select patients with stable New York Heart Association class III or IV heart failure. If angiotensin-converting enzyme inhibitors are not tolerated, angiotensin receptor blockers, hydralazine hydrochloride, and isosorbide dinitrate are recommended. The data on antiarrhythmic and anticoagulation therapies are inconclusive.

Adrenergic beta-Antagonists↗
PubMed2000

Effect of heart failure program on cardiovascular drug utilization and dosage in patients with chronic heart failure.

BACKGROUND: Utilization and dosage of angiotensin-converting enzyme (ACE) inhibitors in patients with chronic heart failure (CHF) remain low. Recent data suggest that care of patients with CHF in specialized heart failure programs is associated with improved clinical outcomes. HYPOTHESIS: Specialized heart failure care is associated with better utilization and higher dose of cardiovascular drugs. METHODS: Data from 133 patients with CHF referred to a heart failure program were analyzed. Mean functional class 3.1 +/- 0.5, left ventricular ejection fraction 19 +/- 8. Utilization and doses of cardiovascular drugs were examined at initial evaluation and at last visit, after an average period of 17 +/- 14 months. Hospitalization and survival data were determined. RESULTS: Utilization of ACE inhibitors and angiotensin-receptor blockers increased from 87 to 100% (p < 0.001). Average daily dose increased by 60%, from the equivalent of captopril 105 +/- 78 mg to 167 +/- 86 mg (p < 0.001). Utilization of the following drugs increased significantly: beta blockers (16-37%, p < 0.001), metolazone (10-23%, p = 0.007), spironolactone (1-36%, p < 0.001), amiodarone (7-15%, p = 0.05), hydralazine (1-9%, p = 0.004), and nitrates (20-33%, p = 0.03). One-year survival was 90%. The 3- and 6-month hospitalization rates for heart failure were 4 and 7%, and for all cardiovascular causes they were 6 and 11%, respectively. CONCLUSIONS: Care of patients with CHF in a specialized heart failure program was associated with significant increase in the utilization and doses of all beneficial cardiovascular drugs, especially ACE inhibitors. It was also associated with excellent clinical outcomes.

Adult↗
PubMed2004

Expression of brain natriuretic peptide in the rat heart studies during heart growth and in relation to sympathectomy.

Brain natriuretic peptide (BNP) might be of importance during heart development and is described to be increasingly expressed in congestive heart failure and to affect the progress of this condition. However, details in the normal expression of BNP are still unclear in various parts of the adult and growing heart, including the conduction system. In this study, we investigated the expression of BNP in relation to that of atrial natriuretic peptide (ANP) in the growing as well as in the adult rat heart. The effects of chemical sympathectomy in adult rats were also examined. Contrary to previous BNP immunohistochemical studies, the BNP antiserum was preabsorbed with an excess of ANP before staining to abolish the crossreactivity with ANP. There was a pronounced BNP immunoreaction in the auricles, the trabeculated ventricular walls, and the peripheral parts of the conduction system at 0-1 days postnatally. The degree of immunoreaction gradually decreased with increasing age. A similar developmental pattern was seen concerning ANP expression, but the magnitude of the latter clearly exceeded that for BNP. Immunoreaction for BNP was never detected in the atrioventricular (AV) node and AV bundle at any stage. In contrast to the situation for ANP previously observed, no obvious changes in BNP immunoreaction patterns were observed in response to sympathectomy. This is the first study to thoroughly demonstrate the expression of BNP in the various regions of the rat heart during growth and in the normal and sympathectomized adult stage. The observations are related to possible functions of natriuretic peptides in the growing and adult heart.

Animals↗
PubMed1996

A work-performing heart preparation for myocardial performance analysis in murine hearts.

UNLABELLED: The mouse has become the animal of choice for genetic manipulations resulting in altered myocardial function, but assessment of cardiac function is extremely difficult due to the animal's size. This study was designed to establish a work-performing isolated mouse heart preparation to objectively investigate myocardial performance in murine hearts. Isolated work-performing cardiac functional studies were performed on a modified Langendorff apparatus using 15 mice [25 to 28 g, +/-0.4 (SEM)]. The hearts were instrumented with a transonic flow meter and micromanometers to measure on-line aortic flow (AF), aortic pressure, and left atrial pressure (preload). A VAX cardiac function analyzing system was used to determine cardiac parameters including heart rate, contractility (max dP/dt), stroke volume (SV), and stroke work (SW) at various preload levels compared to a baseline preload of 5 mm Hg before and after 7 min of warm ischemia. AF increased from 1.01 ml/min (+/- 0.26) at 5 mm Hg of preload to 4.15 ml/min (+/- 1.03, P < 0.05) at 20 mm Hg of preload and decreased to 3.64 ml/min (+/- 0.62) at 25 mm Hg. SV, dP/dt, and SW increased with higher preload levels. There was a significant decrease in cardiac function postischemia. CONCLUSIONS: A valid isolated work-performing preload-dependent murine heart preparation involving minimal instrumentation of the heart is established to measure cardiac function and myocardial performance. Significant ischemia-reperfusion injury occurred after 7 min of ischemia. This model is a reliable and objective tool by which to evaluate murine cardiac function and to study ischemia-reperfusion injury.

Animals↗
PubMed1998

Complete coding sequence of inducible nitric oxide synthase from human heart and skeletal muscle of patients with chronic heart failure.

The presence of the inducible nitric oxide synthase (iNOS) has previously been reported in heart and skeletal muscle of patients with chronic heart failure, where it is thought to be involved in the pathogenesis of dilated cardiomyopathy or of exercise intolerance observed in patients with chronic heart failure. To identify the iNOS of these human tissues the cDNA sequence was determined using reverse transcription polymerase chain reaction (RT-PCR). The deduced amino acid sequence of human heart and skeletal muscle shows a 99% identity between each other. The amino acid sequence was distinct from the constitutively expressed nitric oxide synthases. A 98% identity at the protein level was detected to rat vascular smooth muscle iNOS, whereas the homology to human hepatocyte iNOS was only 79%. The cofactor binding sites in the reported iNOS from human heart and skeletal muscle are highly conserved. The iNOS sequence described in this report is the first one isolated directly from human tissue expressing iNOS in the circumstances of chronic heart failure.

Amino Acid Sequence↗
PubMed1992

Does changing the heart mean changing personality? A retrospective inquiry on 47 heart transplant patients.

Heart transplantation is not simply a question of replacing an organ that no longer functions. The heart is often seen as source of love, emotions, and focus of personality traits. To gain insight into the problem of whether transplant patients themselves feel a change in personality after having received a donor heart, 47 patients who were transplanted over a period of 2 years in Vienna, Austria, were asked for an interview. Three groups of patients could be identified: 79% stated that their personality had not changed at all postoperatively. In this group, patients showed massive defense and denial reactions, mainly by rapidly changing the subject or making the question ridiculous. Fifteen per cent stated that their personality had indeed changed, but not because of the donor organ, but due to the life-threatening event. Six per cent (three patients) reported a distinct change of personality due to their new hearts. These incorporation fantasies forced them to change feelings and reactions and accept those of the donor. Verbatim statements of these heart transplant recipients show that there seem to be severe problems regarding graft incorporation, which are based on the age-old idea of the heart as a centre that houses feelings and forms the personality.

Adolescent↗
PubMed1975

[Influence of heart work and substrate uptake on the regulation of pyruvate dehydrogenase activity in isolated guinea pig hearts (author's transl)].

In isolated guinea pig hearts performing a defined stroke work, the influence of heart work and substrate uptake on the interconversion of pyruvate dehydrogenase (PDH) was studied. When hearts from fasted animals are perfused with a salt solution containing 10mM glucose, an increase in cardiac output and aortic pressure effects an increase in active PDH from 50 to 74% of total PDH activity and a decrease in tissue content of energy-rich phosphates. Pyruvate turnover calculated from oxygen consumption corresponds with PDH activity. Under these experimental conditions, PDH activity might either represent the rate limiting step of oxidative glucose breakdown, or it might be adjusted to a flux rate controlled by other factors. In fed animals, PDH activity exceeds the pyruvate turnover. However, an increase of heart work raises the active PDH from 76 to 95%. Addition of 10 mM acetate to the perfusion medium decreases PDH activity and glucose uptake. In fed animals, an increase of heart work raises the active PDH from 43 to 59% only, whereas in fasted animals this effect is abolished. The effect of changes in heart work on PDH interconversion might be explained by changes in energy-rich phosphate concentrations. However, substrate uptake and nutritional state may interfere or even abolish this effect.

Acetates↗
PubMed1983

Acute effects of alinidine on heart rate and blood pressure in healthy subjects and patients with hyperkinetic heart syndrome.

The effects of a single dose of alinidine (0.5 mg/kg i.v.), the N-allyl-derivative of clonidine, on heart rate and blood pressure were investigated in healthy volunteers and in patients with hyperkinetic heart syndrome, at rest and during bicycle exercise. In healthy volunteers plasma catecholamine levels were also determined. Alinidine did not change heart rate at rest in the healthy volunteers but it did significantly reduce exercise-induced tachycardia, whereas blood pressure and plasma catecholamine levels were not significantly affected by alinidine, either at rest or during exercise. In patients with hyperkinetic heart syndrome, alinidine reduced heart rate at rest and during exercise to a similar extent as propranolol (0.1 mg/kg i.v.). The blood pressure did not change with alinidine but it was significantly reduced by propranolol. The observation that an alinidine-induced reduction of heart rate occurs without a concomitant fall in blood pressure, and without a clonidine-like symphatho-inhibitory action, is in line with experimental findings suggesting a specific bradycardic action of alinidine under short-term conditions.

Blood Pressure↗
PubMedDate not supplied

Hemodynamic correlates of baroreflex impairment of heart rate in experimental canine heart failure.

The arterial baroreflex has been shown to be depressed in both clinical and experimental heart failure. The mechanism and significance of this depression remains controversial. Part of the change may reside in the baroreceptor as well as in the target organ. Previous studies in this laboratory have shown that there is no central depression of the baroreflex in anesthetized dogs. The present study was undertaken to determine the relationship between the change in baroreflex sensitivity (BRS) and the impairment of various hemodynamic parameters during the development of chronic heart failure in conscious dogs (n = 15). The animals were instrumented to record pressures and derivatives in the left atrium, aorta and the left ventricle. Heart failure was achieved by rapid left ventricular pacing (250 bpm) until the development of clinical signs. BRS was determined by correlating systolic arterial blood pressure and pulse interval during bolus injections of nitroglycerin and phenylephrine. Data were analyzed by correlating the changes in BRS (n = 90) with respect to changes in each parameter. No or a weak correlation was found between the changes in the baroreflex and parameters of systolic function or time of pacing. A stronger correlation was found between BRS and parameters of preload such as left ventricular enddiastolic pressure and left atrial pressure (p < 0.001). In general, the bradycardia responses were depressed less than the tachycardia responses. The correlation between BRS and left atrial or left ventricular end diastolic pressure is consistent with the view that augmented input from cardiac receptors may contribute to the depressed baroreflex function in heart failure. These data also suggest that the sympathetic limb of baroreflex control of heart rate in chronic heart failure is depressed earlier and to a greater extent then the vagal limb.

Animals↗
PubMed1994

Effects of saterinone and its enantiomers R(+)-saterinone and S(-)-saterinone on the phosphodiesterase isoenzymes from ventricular tissue of failing human hearts and porcine hearts.

Stereoisomers often exhibit differences in their pharmacological activities. Therefore, the phosphodiesterase inhibitory effects of the cardiotonic agent saterinone in form of the racemate were investigated in comparison with the inhibitory properties of its enantiomers R(+)- and S(-)-saterinone. For this purpose the phosphodiesterase isoenzymes from ventricular tissue of failing human hearts and porcine hearts were separated by DEAE-sepharose anion exchange chromatography. Four different phosphodiesterase isoenzymes were isolated from failing human myocardium and designated phosphodiesterase I-IV. Three phosphodiesterase isoenzymes could be separated from ventricular tissue of porcine hearts. A Ca2+/calmodulin stimulated phosphodiesterase I was not detectable in porcine myocardium. In failing human hearts racemic saterinone was a potent inhibitor of phosphodiesterase III (IC50 0.02 mumol/l) and IV (IC50 0.03 mumol/l) as compared to the inhibition of phosphodiesterase I (IC50 37.3 mumol/l) and II (IC50 51.4 mumol/l). In comparison with the racemate, R(+)- and S(-)-saterinone showed only slight differences in their phosphodiesterase inhibitory effects. R(+)-saterinone inhibited phosphodiesterase III slightly but significantly more potently and selectively than did S(-)-saterinone. Compared to the inhibition of phosphodiesterase I and II both enantiomers were similarly potent and selective inhibitors of phosphodiesterase III and IV. Similar results were obtained in porcine hearts. It is concluded that the racemate saterinone and its enantiomers (R(+)- and S(-)-saterinone are virtually equipotent concerning the inhibition of phosphodiesterase isoenzymes isolated from failing human hearts or porcine ventricular tissue. The enantiomers of saterinone did not exhibit distinct stereoselectivity in their phosphodiesterase inhibitory effects.

1-Methyl-3-isobutylxanthine↗
PubMedDate not supplied

Thin myofilament proteins in norm and heart failure. I. Polymerizability of myocardial Straub actin in acute and chronic heart failure.

The reduced and intrinsic viscosities of myocardial Straub F-actin from the left ventricle of a practically healthy man were equal to 3.05 +/- 0.2 and 2.4 +/- 0.32 and from the right ventricle were 2.37 +/- 0.2 and 2.1 +/- 0.3 dl/g, respectively (the difference between ventricles was not significant). The average length of filaments measured by flow birefringence technique was equal to 1.3 +/- 0.04 micron, the number-average length (Ln), determined by the electron microscopy was 1.4 micron, the weight-average length (Lw), was 2 microns and the maximal one was 5.5 microns. The histograms showed that the most characteristic length was that of 0.8-1.2 micron. According to the flow birefringence data canine myocardial F-actin had a length similar to that of myocardial F-actin from a practically healthy man, though its reduced and intrinsic viscosities were higher. In acute and especially chronic congestive heart failure the actin polymerizability was sharply reduced. In consequence, in acute heart failure the number-average length of F-actin filaments was decreased by 43% and in congestive heart failure by 65.7%. The characteristic length in acute heart failure shifts to the range of 0.2-0.6 micron, while in congestive heart failure the range is 0.2-0.4 micron. This fact can possibly explain why during preparation of actin from the pathologically changed myocardium according to the methods including purification by the cycles of polymerization-sedimentation-depolymerization, the pathologically changed actin is discarded and the normal actin remains. A definite parallel was observed between the reduction of actin polymerizability and the ability of myocardial glycerinated fiber bundles (MBGF) to generate force. We conclude that the changes of actin properties in heart failure may cause a decrease in contractibility of the myocardial contractile protein system.

Actins↗
PubMed2005

Ischemia-reperfusion leads to depletion of glutathione content and augmentation of malondialdehyde production in the rat heart from overproduction of oxidants: can caffeic acid phenethyl ester (CAPE) protect the heart?

During restoration of blood flow of the ischemic heart induced by coronary occlusion, free radicals cause lipid peroxidation with myocardial injury. Lipid peroxidation end-products, such as malondialdehyde (MDA), have been used to assess oxygen free radical-mediated injury of the ischemic-reperfused (I/R) myocardium in rats. This experimental study assessed the preventive effect of caffeic acid phenthyl ester (CAPE), antioxidant, on I/R-induced lipid peroxidation in the rat heart. We are also interested in the role of CAPE on glutathione (GSH) levels, an antioxidant whose levels are influenced by oxidative stress. I/R leads to the depletion of GSH which is the major intracellular nonprotein sulphydryl and plays an important role in the maintenance of cellular proteins and lipid in their functional state and acts primarily to protect these important structures against the threat of oxidation. In addition, we also examined morphologic changes in the heart by using light microscopy. The left coronary artery was occluded for 30 min and then reperfused for 120 min more before the experiment was terminated. CAPE (50 microM kg(-1)) was administered 10 min prior to ischemia and during occlusion by infusion. At the end of the reperfusion period, rats were sacrificed, and the heart was quickly removed for biochemical determination and histopathological analysis. I/R was accompanied by a significant increase in MDA production and decrease in GSH content in the rat heart. Administration of CAPE reduced MDA production and prevented depletion of GSH content. These beneficial changes in these biochemical parameters were also associated with parallel changes in histopathological appearance. These findings imply that I/R plays a causal role in heart injury due to overproduction of oxygen radicals or insufficient antioxidant and CAPE exert cardioprotective effects probably by the radical scavenging and antioxidant activities.

Animals↗
PubMed1983

The floating heart or the heart too fat to sink: analysis of 55 necropsy patients.

Certain clinical and morphologic findings are described in 55 patients whose hearts at necropsy contained so much fat that they floated in water. The patients were 47 to 89 years old (mean 67). Symptomatic coronary heart disease was present in 28 (51%) and valvular heart disease (mitral stenosis) in 3 (5%). The heart at necropsy was enlarged (greater than 350 g for women and greater than 400 g for men) in 45 patients (82%). The mean heart weight for the 31 women was 470 g and for the 24 men, 515 g. In addition to the severe increase in fat in the atrioventricular sulci and over both ventricles, the amount of fat in the atrial septum was increased in all patients. In 14 patients (25%), the thickness of the atrial septum cephaled to the fossa ovale was greater than or equal to 2 cm. Excessive fat in this location is called "lipomatous hypertrophy of the atrial septum." Of the 16 patients (29%) with fatal acute myocardial infarction, 7 (44%) had rupture of either the left ventricular free wall or ventricular septum. The high frequency of cardiac rupture in these patients supports the contention that rupture during acute myocardial infarction is more common in the fatty than in the non-fatty heart.

Adipose Tissue↗