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At least 361 records · Page 20Linked to original sources
PubMed1993

Clinical consequences of angiotensin-converting enzyme inhibitor withdrawal in chronic heart failure: a double-blind, placebo-controlled study of quinapril. The Quinapril Heart Failure Trial Investigators.

OBJECTIVES: This study was performed to assess the efficacy, safety and clinical consequences of abrupt cessation of quinapril therapy in a placebo-controlled, randomized, double-blind withdrawal trial. BACKGROUND: Angiotensin-converting enzyme inhibitor therapy has assumed a pivotal role in the treatment of chronic heart failure. Quinapril hydrochloride, a nonsulfydryl angiotensin-converting enzyme inhibitor, has shown beneficial clinical effects in previous studies. METHODS: After > or = 10 weeks of single-blind quinapril therapy, 224 patients with New York Heart Association class II or III heart failure were randomized in double-blind fashion to continue quinapril (n = 114) or to receive placebo (n = 110) for 16 weeks. Changes in treadmill exercise time, New York Heart Association functional class, quality of life and symptoms of heart failure were assessed. RESULTS: Patients withdrawn to placebo had a significant deterioration in exercise tolerance (median change -16 s with placebo vs. +3 s with quinapril, p = 0.015). New York Heart Association functional class (p = 0.004) and quality of life were improved and signs and symptoms of congestive heart failure were lessened in those remaining on quinapril therapy compared with those receiving placebo. During double-blind treatment, 18 patients were withdrawn from the placebo group because of worsening heart failure compared with 5 patients withdrawn from quinapril treatment (p < 0.001). Rather than a precipitous deterioration of clinical status or early incidence of adverse events, withdrawal from quinapril was associated with steady worsening of heart failure, beginning 4 to 6 weeks after randomization to placebo. CONCLUSIONS: Quinapril is effective and safe for maintaining clinical stability in patients with moderate congestive heart failure. Withdrawal of quinapril from patients with heart failure results in a slow progressive decline in clinical status.

Aged↗
PubMed1996

Predictive power of increased heart rate versus depressed left ventricular ejection fraction and heart rate variability for risk stratification after myocardial infarction. Results of a two-year follow-up study.

OBJECTIVES: The aim of this study was to compare the predictive value of mean RR interval assessed from predischarge Holter recordings with that of heart rate variability and left ventricular ejection fraction for risk stratification after myocardial infarction. BACKGROUND: Heart rate variability is a powerful tool for risk stratification after myocardial infarction. Although heart rate variability is related to heart rate, little is known of the prognostic value of 24-h mean heart rate. METHODS: A total of 579 patients surviving the acute phase of myocardial infarction were followed up for at least 2 years. Predischarge heart rate variability, 24-h mean RR interval and left ventricular ejection fraction were analyzed. RESULTS: During the first 2 years of follow-up, there were 54 deaths, 42 of which were cardiac (26 sudden). Shorter mean RR interval was a better predictor of all-cause mortality as well as cardiac and sudden death than depressed left ventricular ejection fraction. Depressed heart rate variability predicted the risk of death better than mean RR interval for sensitivities < 40%. For sensitivities > or = 40%, mean RR interval was as powerful as heart rate variability. All three variables performed equally well in predicting nonsudden cardiac death. For cardiac death prediction, a left ventricular ejection fraction < 35% had a 40% sensitivity, 78% specificity and 14% positive predictive accuracy; a mean RR interval < 700 ms had a 45% sensitivity, 85% specificity and 20% positive predictive accuracy; and a heart rate variability < 17 U had a 40% sensitivity, 86% specificity and 20% positive predictive accuracy. CONCLUSIONS: Predischarge 24-h mean heart rate is a strong predictor of mortality after myocardial infarction that can compete with left ventricular ejection fraction and heart rate variability.

Cohort Studies↗
PubMed2004

Interleukin-6 and B-type natriuretic peptide are independent predictors for worsening of heart failure in patients with progressive congestive heart failure.

BACKGROUND: Neurohormones and cytokines have been associated with poor prognosis in patients with congestive heart failure. However, direct comparisons between them are rare and the best predictor for worsening of heart failure remains to be elucidated. The aim of the study was to identify independent predictors for worsening of heart failure. METHODS: We studied 100 patients with congestive heart failure (LVEF <or=25%). Serum levels of interleukin-6 (IL-6), tumor necrosis factor (TNF)-alpha, aminoterminal atrial natriuretic peptide (N-ANP), B-type natriuretic peptide (BNP), aminoterminal B-type natriuretic peptide (N-BNP), norepinephrine (NE) and big endothelin (big ET) were measured at entry into the study. Univariate and stepwise multivariate regression analyses were performed to compare variables and clinical parameters. The end-point was defined as worsening of heart failure. RESULTS: During follow-up (mean 378 days), 30 patients reached the defined end-point. Univariate risk factors of worsening of heart failure were IL-6 (p = 0.0001), log BNP (p = 0.0001), log N-ANP (p = 0.0259), big ET (p = 0.0032), log N-BNP (p = 0.0495), NE (p = 0.0013) and LVEF (p = 0.0498). Multivariate regression analysis identified IL-6 as the strongest independent predictive value for worsening of heart failure (p = 0.0001), followed by log BNP (p = 0.0002). Mean IL-6 levels were 1.76 +/- 1.73 in stable patients and 4.62 +/- 7.98 pg/ml in patients who developed worsening of heart failure. Using a cut-off value of 1.66 pg/ml for IL-6 Kaplan-Meier freedom from worsening, heart failure was significantly higher in patients below this cut-off point compared with those above (p = 0.0002). CONCLUSIONS: IL-6 and BNP independently predict worsening of heart failure. A single measurement could help to identify patients at high risk for worsening of heart failure and these individuals should be monitored more closely.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2005

Potential suitability for transplantation of hearts from human non-heart-beating donors: data review from the Gift of Life Donor Program.

BACKGROUND: Organ availability limits use of heart transplantation for treatment for end-stage heart disease. Hearts are currently obtained from donors declared brain dead (heart-beating donors [HBDs]). Although use of hearts from non-heart-beating donors (NHBDs) could reduce the shortage, they are considered unusable because of possible peri-mortem ischemic injury. METHODS: To project how use of NHBD hearts could increase heart donation, we retrospectively reviewed donor databases from the Gift of Life Donor Program (GLDP), our local organ procurement organization, from 2001 through 2003. We screened the NHBD population using conservative donor criteria, assuming an acceptable hypoxic/ischemic time (time from withdrawal of care to cross-clamp) of 30 minutes. RESULTS: During the study period, there were 894 HBDs, 334 heart transplants and 119 NHBDs. NHBDs were similar to HBDs with respect to gender and ethnicity, but NHBDs were proportionately younger. Of 119 NHBDs, 55 did not meet the age criteria (< or =45 years) and 20 were eliminated because of incomplete data. Eighty-two NHBDs were cross-clamped within 30 minutes of care withdrawal. Twenty NHBDs met all cardiac donor criteria, and 14 of these 20 had hypoxic/ischemic times < or =30 minutes. Pro rata estimation for the 20 NHBDs with incomplete data suggested 7 potential additional donors. CONCLUSIONS: Based on our assumptions, 12% to 18% of NHBDs in the study period (14 to 21 of 119 total) were potential heart donors, representing a 4% to 6% increase over of the number of heart transplants performed during the same time interval.

Adolescent↗
PubMed2006

An adjunctive preventive treatment for heart disease and a set of diagnostic tests to detect it: insulin-like growth factor-1 deficiency and cell membrane pathology are an inevitable cause of heart disease.

Coronary heart disease (CHD) is a preventable disease with high morbidity and mortality. Largely omitted from the efforts at detection and treatment are the contributions of the lungs, the skeletal muscles and the arteries to heart disease pathology. Also omitted are the effects of the age-related decline in insulin-like growth factor-1 (IGF-1) and the age-related increase in cell membrane pathology. The hypothesis on which this model is based postulates that growing older, over time, necessarily results in pathological changes in the heart, the lungs, the skeletal muscles and the arteries. Additionally, the age-related decline in (IGF-1) that occurs in the otherwise healthy aged population also causes similar pathological changes. The drug portion of the proposed treatment includes the use of the drug acetyl-l-carnitine (ALC) to increase the age-related decreased IGF-1 levels. The drug centrophenoxine (CPH) is used to reverse the age-related pathological changes that inevitably occur in the heart, the lungs, the skeletal muscles and the arteries. A testing procedure is included to improve the detection of heart disease and to monitor the results. It consists of five tests: the monitoring of plasma IGF-1 levels; the monitoring of blood pressure, and in particular elevated systolic blood pressure; the monitoring of blood pressure variability over time; a heart rate recovery time test and a heart rate reserve test. Heart rate reserve is defined as the difference between maximal heart rate and resting heart rate, after treadmill exercise. The changes in test results noted during treatment are an indicator of progress or deterioration in the prevention of heart disease, whatever the case may be.

Blood Pressure↗
PubMed1998

Heart rate variability and heart rate in healthy volunteers. Is the female autonomic nervous system cardioprotective?

AIMS: Heart rate variability has been proposed as an indicator of cardiovascular health. Since women have a lower cardiovascular risk, we hypothesized that there are gender differences in autonomic modulation. METHODS AND RESULTS: In 276 healthy subjects (135 women, 141 men) between 18 and 71 years of age, 24 h heart rate and heart rate variability were determined. All heart rate variability parameters, except for pNN50 and high frequency power, were higher in men. After adjustment for heart rate, we obtained gender differences for: the standard deviation (P=0.049), the standard deviation of the 5 min average (P=0.047), low frequency power (absolute values, P=0.002; normalized units, P<0.001) and ratio low frequency/high frequency (P<0.001). There were no significant gender differences in heart rate variability parameters denoting vagal modulation. Gender differences were confined to age categories of less than 40 years of age. The majority of heart rate variability parameters decreased with age. Only in men, was a higher body mass index associated with a higher heart rate and with lower heart rate variability parameters (P<0.001). CONCLUSION: Cardiac autonomic modulation as determined by heart rate variability, is significantly lower in healthy women compared to healthy men. We hypothesize that this apparently paradoxical finding may be explained by lower sympathetic activity (low frequency power) in women. This may provide protection against arrhythmias and against the development of coronary heart disease.

Adolescent↗
PubMed1993

Minute-by-minute association of heart rate variation with basal heart rate in developing infants.

Particular types of heart rate variation are enhanced during periods of slow heart rate and diminished when heart rate is high. We examined how the correlations between heart rate and various types of heart rate variation developed in normal infants. Polygraphic recordings were obtained from 25 infants at 1 week and at 1, 2, 3, 4 and 6 months of age. Median heart rate and the extents of heart rate variation at three distinct frequencies were determined for each 1-minute epoch. Pearson's r was used to assess the correlation of median heart rate in each epoch with each of three types of heart rate variation. For each recording, correlations were assessed separately for quiet sleep, rapid eye movement (REM) sleep and waking. The maturational patterns of heart rate by heart rate variation correlations were strongly influenced by sleep-waking state and were dissimilar to those previously reported for correlations between cardiac and respiratory measures. The findings suggest dissimilar developmental patterns for autonomic and somatic motor systems, and include a discontinuity in autonomic development at approximately 1 month of age. We speculate that these trends reflect a change in the nature of sleep states as forebrain connections develop.

Aging↗
PubMed2002

Overexpression of A(3) adenosine receptors decreases heart rate, preserves energetics, and protects ischemic hearts.

To determine whether A(3) adenosine receptor (A(3)AR) signaling modulates myocardial function, energetics, and cardioprotection, hearts from wild-type and A(3)AR-overexpressor mice were subjected to 20-min ischemia and 40-min reperfusion while (31)P NMR spectra were acquired. Basal heart rate and left ventricular developed pressure (LVDP) were lower in A(3)AR-overexpressor hearts than wild-type hearts. Ischemic ATP depletion was delayed and postischemic recoveries of contractile function, ATP, and phosphocreatine were greater in A(3)AR-hearts. To determine the role of depressed heart rate and to confirm A(3)AR-specific signaling, hearts were paced at 480 beats/min with or without 60 nmol/l MRS-1220 (A(3)AR-specific inhibitor) and then subjected to ischemia-reperfusion. LVDP was similar in paced A(3)AR-overexpressor and paced wild-type hearts. Differences in ischemic ATP depletion and postischemic contractile and energetic dysfunction remained in paced A(3)AR-overexpressor hearts versus paced wild-type hearts but were abolished by MRS-1220. In summary, A(3)AR overexpression decreased basal heart rate and contractility, preserved ischemic ATP, and decreased postischemic dysfunction. Pacing abolished the decreased contractility but not the ATP preservation or cardioprotection. Therefore, A(3)AR overexpression results in cardioprotection via a specific A(3)AR effect, possibly involving preservation of ATP during ischemia.

Adenosine Triphosphate↗
PubMed1996

Blockade of AT1 receptors enhances baroreflex control of heart rate in conscious rabbits with heart failure.

Because the renin-angiotensin system is activated in heart failure, we hypothesized that angiotensin II (ANG II) plays a role in altering baroreflex sensitivity in the setting of heart failure. Accordingly, we evaluated the baroreflex control of heart rate (HR) in conscious, chronically instrumented rabbits in the normal state and after the establishment of heart failure. Heart failure was induced by rapid ventricular pacing at a rate of 360-380 beats/min for an average of 14.5 +/- 1.4 days. The data were compared with normal rabbits instrumented in a similar fashion. Baroreflex curves were generated by inflation of implanted hydraulic occluders on the vena cava and aortic arch or by administration of phenylephrine and sodium nitroprusside. Experiments were carried out before and after intravenous administration of the AT1 antagonist L-158,809. Rabbits with heart failure exhibited significantly lower arterial pressure (81 +/- 3 vs. 69 +/- 4 mmHg, P < 0.05), elevated resting HR (230 +/- 5 vs. 260 +/- 10 beats/min, P < 0.05), and elevated left atrial pressure (3.6 +/- 0.7 vs. 13.1 +/- 0.7 mmHg, P < 0.05). ANG II blockade had little effect on resting or baroreflex parameters in normal rabbits. However, in rabbits with heart failure, L-158,809 enhanced baroreflex sensitivity (2.7 +/- 0.5 vs. 4.7 +/- 0.8 beats.min-1.mmHg-1; P < 0.05), primarily by increasing the minimum HR evoked during baroreceptor activation. beta 1-Blockade had no effect on any baroreflex parameter after L-158,809 in rabbits with heart failure. However, L-158,809 significantly reduced the minimum HR after pretreatment with atropine in rabbits with heart failure. These data suggest that ANG II plays a role in modulation of cardiac sympathetic tone in this model of heart failure and may be responsible for the depressed baroreflex sensitivity observed in heart failure.

Angiotensin Receptor Antagonists↗
PubMed1995

Expression of renin-angiotensin system components in the heart, kidneys, and lungs of rats with experimental heart failure.

BACKGROUND: Chronic activation of the renin-angiotensin system (RAS) plays an important role in the pathogenesis of heart failure. Increasing evidence indicates that other than the circulating RAS, a local RAS exists in several tissues, including the heart. The present study was carried out to quantify cardiac, renal, and pulmonary mRNA levels of renin, angiotensin-converting enzyme (ACE), and types 1 and 2 angiotensin II receptors (AT-1 and AT-2), in rats with different severities of heart failure. METHODS AND RESULTS: Heart failure was induced by the creation of an aortocaval fistula below the renal arteries. Rats with aortocaval fistula either compensate and maintain a normal sodium balance or decompensate and develop severe sodium retention. Six days after placement of the aortocaval fistula, heart weight (normalized to body weight) increased 35% (P < .05) in compensated and 65% in decompensated rats compared with control rats. Plasma renin activity increased 45% (P < .05) in rats in sodium balance and 127% in sodium-retaining rats. Total RNA was extracted from the heart, kidneys, and lungs, followed by reverse transcription-quantitative polymerase chain reaction. Renin mRNA levels in the heart, after 40 cycles, increased 68% (P < .01) and 140% in rats with either compensated or decompensated heart failure, respectively. Renal renin-mRNA levels also increased 130% (P < .05) in decompensated and only 52% (P < .05) in compensated animals. ACE-mRNA increased in a similar pattern in the heart but not in either the kidneys or lungs. Moreover, pulmonary, renal, and cardiac ACE immunoreactivity levels, assessed by Western blot analysis, showed the same trend. AT-1 receptor mRNA levels decreased 54% (P < .05) only in the myocardium of decompensated rats, whereas AT-2 receptor mRNA did not change in any tissue studied. CONCLUSIONS: The development of heart failure is associated with a remarkable increase in the expression of a local RAS in the heart, which may contribute to the pathogenesis of this clinical syndrome.

Angiotensin II↗
PubMed1995

Human heart-infiltrating T-cell clones from rheumatic heart disease patients recognize both streptococcal and cardiac proteins.

BACKGROUND: beta-Hemolytic streptococcal infection in developing countries still causes thousands of causes of rheumatic heart disease, demanding surgical valve correction. Antigenic mimicry between self and streptococcal components has been proposed as the triggering factor leading to autoimmunity in individuals with genetic susceptibility. Although heart streptococcal-M protein cross-reactive antibodies have been demonstrated, heart tissue damage seems to be T lymphocyte-dependent. We studied the infiltrating T lymphocytes in rheumatic heart lesions with the aim of understanding the role of cellular immune response at the site of the lesions. METHODS AND RESULTS: We obtained 107 T-cell clones from surgical fragments of cardiac tissue from four rheumatic heart disease patients. We tested their capacity to recognize streptococcal M protein-derived synthetic peptides and heart proteins. We found eight infiltrating T-cell clones from all four patients that simultaneously recognize streptococcal M and heart proteins. Among the M-protein sequences tested, only synthetic peptides corresponding to regions 1 through 25, 81 through 103, and 163 through 177 were simultaneously recognized with heart protein fractions. Interestingly, regions 81 through 103 and 163 through 177 have been known to bear heart cross-reactive epitopes at the antibody level. Five of these clones are CD4+, and one is CD8+. CONCLUSIONS: The presence of heart-M protein cross-reactive T-cell clones in rheumatic heart lesions suggests their direct involvement in the pathogenesis of this disease. The dissection of protective and pathogenic epitopes of streptococcal M protein is an important step in allowing the development of a safe anti-streptococcal synthetic vaccine.

Amino Acid Sequence↗
PubMed1990

Dobutamine potentiates amrinone's beneficial effects in moderate but not in advanced heart failure. 31P-MRS in isolated hamster hearts.

There is controversy as to whether potent inotropic agents are beneficial or detrimental in moderate to severe heart failure. Accordingly, we studied the effects of amrinone, amrinone plus dobutamine, and dobutamine alone on mechanical performance, myocardial oxygen consumption, and high energy phosphate metabolism in different stages of congestive heart failure in the cardiomyopathic Syrian hamster. In hearts with moderate heart failure, administration of amrinone, amrinone plus dobutamine, and dobutamine alone increased developed pressure significantly, whereas the phosphorylation potential increased significantly only with amrinone and amrinone plus dobutamine. In hearts with advanced heart failure, administration of amrinone and amrinone plus dobutamine increased developed pressure significantly, whereas dobutamine alone had no effect. The phosphorylation potential improved significantly only with amrinone. Thus, amrinone improved mechanical performance and mitochondrial activity in both heart failure states. Dobutamine potentiated amrinone's beneficial effects in moderate heart failure, but negated the positive inotropic effect of amrinone in advanced heart failure. Therefore, hearts responded differently to potent inotropic agents depending on the severity of heart failure.

Amrinone↗
PubMed1975

A study on the rehabilitation of ischemic heart disease patients. The heart rate, beta-receptor blocking agents and strength-duration relationship of exercise.

Exercise tests with bicycle ergometer were performed in 9 normals and 54 patients with ischemic heart disease (IHD), in order to evaluate the heart rate (HR) as a parameter for determining the physical working capacity and controlling the daily activities, and to observe the circulatory and metabolic effects of beta-blockers and moreover to study the strength-duration relationship of exertion. The following results were obtained and discussed: 1. Reliable correlation between heart rate and O2 consumption during all phases of exercise, including the recovery period (R = 0.60-0.87, p less than 0.001) and parallelism of heart rate and pressure rate product allows the heart rate to be used as a parameter for myocardial O2 demand and ST-T changes. It is reasonable to evaluate the exercise effect by the net increment of heart rate during and after exercise, and to utilize the increment of heart rate in the recovery period for the evaluation of physical fitness and adaptability. 2. Similar to other studies made on beta-blockers, in this study too, the agents including Kö 1366 suppressed the exercise responses of heart rate (p less than 0.01), the product of heart rate and blood pressure (p less than 0.01), and O2 consumption (p less than 0.01). But a relatively slow recovery of O2 consumption from the peak response towards pre-exercise level and a higher O2 pulse in the early recovery period was observed after beta-blocker medication. 3. Capillary (ear lobe) pH decreased and recovered in correlation with the strength of exertion. This corresponded with the response of other factors such as ST-T, heart rate, pressure-rate product, and O2 consumption, showing that the exercise strength was one of the more dominant factors to determine allowable work load for ischemic heart disease patients. 4. Recovery of pH was delayed after medication with Kö 1366 (p less than 0.01).

Adrenergic beta-Antagonists↗
PubMed2002

Oxygen costs of left ventricular contractility for dobutamine and Ca(2+) in normal rat hearts and the cost for dobutamine in Ca(2+) overload-induced failing hearts.

The aim of the present study was to compare the oxygen (O(2)) cost of left ventricular (LV) contractility (equivalent maximal elastance; eEmax, an index for contractility) for dobutamine (a beta-receptor stimulant) with that for calcium (Ca(2+)) in normal rat hearts and to assess the O(2) cost of LV eEmax for dobutamine in Ca(2+) overload-induced failing rat hearts. The mean O(2) cost of LV eEmax (x10(-4) microl O(2) x beat(-1) x mmHg(-1) x ml x g(-2)) for Ca(2+) was 1.30+/-0.37 in 12 normal hearts, and for dobutamine it was 1.26+/-0.30 in eight different normal hearts. In the same five normal hearts, the mean O(2) cost of LV eEmax for dobutamine was 1.15+/-0.27, and for Ca(2+) it was 0.81+/-0.36. These mean values showed no significant differences between Ca(2+) and dobutamine. In five Ca(2+) overload-induced failing hearts, the mean O(2) cost of LV eEmax for Ca(2+) could not be assessed, but the mean O(2) cost of LV eEmax for dobutamine was 1.04+/-0.40. This mean value for dobutamine did not differ significantly from those (see above 1.26+/-0.30 or 1.15+/-0.27) in the normal hearts. The present results indicate, in terms of the coupling of mechanical work and energetics of the heart, that the total Ca(2+) handling VO(2) in excitation-contraction coupling against unit LV contractility change for dobutamine in the contractile failing hearts does not differ from that in the normal hearts. This suggests that in the Ca(2+) overload-induced contractile failing hearts, there were no changes in the sensitivity of the contractile machinery for Ca(2+), in the Ca(2+)/ATP in the total Ca(2+) handling, and in the ATP/VO(2) in the mitochondria.

Animals↗
PubMed1987

Reconstitution of muscarinic cholinergic inhibition of adenylate cyclase activity in homogenates of embryonic chick hearts by membranes of adult chick hearts.

We have previously demonstrated that during embryonic development of the chick heart between days 2 1/2 and 10 days in ovo, muscarinic cholinergic inhibition of isoproterenol-stimulated adenylate cyclase activity increased 4-fold, and the sensitivity of isoproterenol-stimulated adenylate cyclase activity to inhibition by carbamylcholine increased 26-fold. Although the number of muscarinic receptors remained constant between days 2 1/2 and 10 in ovo, the levels of a 39- and 41-kDa pertussis toxin substrate increased in parallel with the ability of muscarinic agonist to inhibit adenylate cyclase activity (Liang. B.T., Hellmich, M. R., Neer, E. J., and Galper, J. B. (1986) J. Biol. Chem. 261, 9011-9021). These data are consistent with the hypothesis that between days 2 1/2 and 10 in ovo muscarinic receptors were uncoupled from inhibition of adenylate cyclase activity because of limiting levels of pertussis toxin substrates. In the current studies, in order to test this hypothesis homogenates of embryonic chick hearts 3 1/2 days in ovo were reconstituted with membranes from hearts of hatched chicks. In order to rule out reconstitution by factors from hatched chick hearts other than pertussis toxin substrates, muscarinic receptors from hatched chick hearts were inactivated by covalent binding of benzilycholine mustard and adenylate cyclase inactivated by N-ethylmaleimide prior to reconstitution. Reconstitution of benzilylcholine mustard/N-ethylmaleimide treated hatched chick heart membranes with homogenates of embryonic chick hearts 3 1/2 days in ovo resulted in a 2 1/2-fold increase in the ability of carbamylcholine to inhibit adenylate cyclase activity and reconstitution of hatched chick heart membranes with homogenates of hearts 2 1/2 days in ovo resulted in an approximately 10-fold increase in the sensitivity of isoproterenol-stimulated adenylate cyclase activity to inhibition by carbamylcholine. Membranes from hearts of hatched chicks which had been injected with pertussis toxin were incapable of reconstituting muscarinic inhibition of adenylate cyclase activity in homogenates of hearts 3 1/2 days in ovo. These data support the conclusion that early in embryonic development coupling of muscarinic receptors to inhibition of adenylate cyclase activity is limited by the availability of a pertussis toxin substrate.

Adenylate Cyclase Toxin↗
PubMed1984

Metabolic blocker-induced cell damage in rat cardiac tissue. Comparison of three models currently used: the isolated perfused heart, heart cell cultures and isolated myocytes.

In a comparative study on metabolic blockade-induced cardiac cell damage, three different heart (cell) preparations are exposed to potassium cyanide (KCN) and iodoacetamide (IAA) in fixed concentrations (5 and 0.1 mmol/l, respectively). The preparations used are the perfused rat heart, isolated rat heart myocytes and rat heart cell cultures. Irreversible heart cell damage is reflected by the release of a cytoplasmic enzyme, LDH (lactate dehydrogenase), or HBDH (alpha-hydroxybutyrate dehydrogenase) from the heart (cell) preparations. Metabolic blockade-induced release of 50% of the originally intracellularly located LDH or HBDH is reached after 2-3 h from rat heart cell cultures, after 2-4 h from isolated rat heart myocytes and after variable (coronary flow-dependent) durations of perfusion from perfused rat hearts. It is concluded that to study the effect of toxic agents on myocytic integrity, the use of isolated cardiac myocytes and heart cell cultures is preferable to the use of isolated perfused hearts.

Animals↗
PubMed2000

Nuchal translucency and congenital heart defects: heart failure or not?

OBJECTIVE: To determine whether heart failure is the mechanism underlying the association between increased fetal nuchal translucency and congenital heart defects. METHODS: Retrospective analysis of the types of congenital heart defect observed in fetuses with increased nuchal translucency and those with normal nuchal scans. Retrospective quantitative analysis of cardiac size and left ventricular ejection fraction in fetuses with ventricular septal defects or the hypoplastic left heart syndrome. RESULTS: Eighty-three fetuses with congenital heart defects had undergone nuchal screening of which 51 had increased nuchal translucency and 32 had normal nuchal translucency. A wide variety of different congenital cardiac lesions with different hemodynamic effects were observed in fetuses with increased nuchal translucency and those with normal nuchal scans. Defects primarily characterized by left heart obstruction, right heart obstruction and septal defects occurred in both groups. All measurements of cardiothoracic ratio and left ventricular ejection fraction fell within the normal range and there was no significant difference between fetuses with increased nuchal translucency and those with normal nuchal scans. CONCLUSIONS: No specific type of congenital heart lesion is associated with increased nuchal translucency. The contention that heart failure explains the association between congenital heart defects and increased nuchal translucency is not supported by this study.

Heart Defects, Congenital↗
PubMed1998

Spectral analysis of heart valve sound for detection of prosthetic heart valve diseases.

The spectral analysis of heart valve sound is a noninvasive diagnostic method known to be useful in evaluating the state of the heart valve function. This may provide early detection of valve calcification, thrombus or destruction, since previous studies have shown that the dominant frequency peak moved to a high frequency area when natural heart valve leaflets were calcified, stiffened or destroyed. However, it is important for a heart valve sound diagnostic system to find a proper spectral analysis method on phonocardiography. Until now, conventional frequency analyses such as the Fourier transform or autoregressive spectral estimation technique have been used to estimate spectral components of a phonocardiogram, but they are inappropriate because the signal frequency is assumed to remain constant during the transform interval. To overcome this problem, in this study, FOS (Fast Orthogonal Search) & MUSIC (MUltiple SIgnal Classification), which both appeared suitable for the analysis of biological data, were applied to prosthetic heart valve sound as the new heart valve sound spectral analysis methods. Five subjects with normally functioning mechanical heart valves and a patient with a malfunctioning one were selected to collect the heart valve sound signals. As a result, the second dominant peak frequency proved to be important along with the first dominant peak frequency in identifying the valve function. This study showed that the new heart valve sound spectral analysis method presented in this paper may be an effective method in heart valve sound analysis. Further study using this system in a large population of patients will aid in providing a diagnostic method in the early detection of valve failure.

Female↗