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At least 1,135 records · Page 63Linked to original sources
PubMed1984

Cardiac function in alcoholics with cirrhosis: absence of overt cardiomyopathy--myth or fact?

Cardiomyopathy in alcoholics is considered to be associated with a low incidence of hepatic cirrhosis. To evaluate cardiac hemodynamics in alcoholic liver disease, left ventricular function in 37 patients with hepatic cirrhosis (group II) was compared with that in 13 normal subjects (group I) matched for age, sex and cardiac size. These groups were contrasted with group III, comprising 32 alcoholics without cirrhosis who had cardiac symptoms but no cardiomegaly or heart failure. Patients with cirrhosis as a group did not differ from normal subjects (group I) in terms of left ventricular filling pressure and cardiac muscle and pump function (cardiac index). However, subgroup IIA (n = 21) had a stroke index significantly less than normal, while subgroup IIB had a significantly increased stroke index and myocardial cardial contractility with a diminished systemic arterial resistance. Similar hepatic abnormalities were present in both subgroups. In group III, left ventricular end-diastolic and aortic mean pressures were significantly elevated compared with values in normal subjects, while cardiac index and indexes of ventricular contraction and relaxation were abnormal. Further examination of patients with cirrhosis indicated that the responses to volume or pressure increments in terms of the level of stroke work for a given filling pressure were most abnormal in group IIA, approximating those of group III. Thus, although overt cardiomyopathy is infrequent in patients with cirrhosis, asymptomatic myocardial disease may assume clinical importance during volume or pressure overload.

Blood Pressure↗
PubMed2005

Phospholamban: a key determinant of cardiac function and dysfunction.

Our knowledge and understanding of the normal and diseased heart has advanced significantly over the past decade. Evidence indicates that several signaling pathways involved in the induction of cardiac disease and heart failure are associated with abnormal calcium handling by the sarcoplasmic reticulum proteins: calcium-ATPase pump and phospholamban. Indeed, the failing heart is characterized by impaired removal of cytosolic calcium, reduced loading of the cardiac sarcoplasmic reticulum, and defective calcium release, culminating in impairment of cardiac diastolic and systolic function. This review summarizes studies which highlight the key role of the sarcoplasmic reticulum proteins, calcium-ATPase pump and phospholamban, in the regulation of cardiac function; the significance of the phospholamban interaction with the calcium-ATPase pump through transgenic animal models; the recent findings of the inhbitor-1 of protein phosphatase-1 as a new potential therapeutic agent in heart failure; and finally, the discoveries of human phospholamban mutations leading to disease states.

Animals↗
PubMed2000

Lithium has no direct effect on cardiac function in the isolated, perfused rat heart.

To determine if lithium exerts direct cardiac toxicity, using an isolated, perfused rat heart model, paced and unpaced beating rat hearts were perfused with Krebs-Henseleit bicarbonate solution and left ventricular pressures were measured via a balloon-tipped catheter positioned in the left ventricle via the mitral valve. Following a stabilization period, hearts were then perfused with Krebs-Henseleit bicarbonate solution containing 1, 10, and 100 mM ionized lithium chloride or lithium carbonate in an antecedent dose-response protocol and perfused for 10 min. at each dose. To control for the possibility of osmotic effects from the high dose of lithium, an additional group was studied in which hearts were perfused with Krebs-Henseleit bicarbonate solution for an initial stabilization period, then perfused for an additional 20 min. with Krebs-Henseleit bicarbonate solution alone, and finally with Krebs-Henseleit bicarbonate solution containing mannitol (200 mOsm/l) for 10 min. Lithium did not have any effect on left ventricular peak systolic pressure, left ventricular end diastolic pressure, heart rate or coronary haemodynamics at concentrations of 1 or 10 mM. At 100 mM LiCl and Li2CO3, left ventricular peak systolic pressure decreased transiently during the first minute of lithium infusion, but recovered significant function by 10 min. Heart rate decreased significantly by 10 min. of infusion. These effects were also seen in the osmotic controls and thus do not appear to be a direct effect of lithium. At the doses tested, lithium had no direct effect on cardiac function which could not be explained by an osmotic effect.

Analysis of Variance↗
PubMed2006

Histidine-rich Ca binding protein: a regulator of sarcoplasmic reticulum calcium sequestration and cardiac function.

Defects in the pathways that regulate cardiac sarcoplasmic reticulum (SR) calcium (Ca) cycling represent prime targets for driving the deterioration of function and progression to heart failure. We hypothesized that the histidine-rich Ca binding protein (HRC) in the SR may be involved in SR Ca cycling and that alterations in HRC levels would result in abnormal cardiac Ca homeostasis. In order to test this hypothesis, we generated transgenic mice with cardiac overexpression (3-fold) of HRC. Increased cardiac HRC levels were associated with impaired SR Ca uptake rates (35%) and attenuated cardiomyocyte Ca transient decay (38%), without alterations in peak Ca transients or SR Ca load. The depressed SR Ca sequestration was associated with attenuated rate of Ca extrusion via Na-Ca exchange. Triadin protein expression levels and L-type Ca channel current density were increased, while the channel inactivation kinetics were not altered. Impaired SR Ca uptake and delayed Ca decline rates triggered hypertrophy and compromised the heart's responses to increased stress by either hemodynamic overload or the aging process. By 18 months of age, cardiac remodeling deteriorated to congestive heart failure in transgenic mice. Collectively, these data suggest that HRC may be an integral regulatory protein involved in cardiac muscle SR Ca uptake and Ca homeostasis.

Animals↗
PubMed1992

The protective effect of puerarin against myocardial reperfusion injury. Study on cardiac function.

In order to find out if puerarin could protect the hearts from myocardial reperfusion injury after cardiac arrest, twelve dogs divided into two equal groups were placed on moderately hypothermic cardiopulmonary bypass and their hearts were subjected to 140 min of cold cardioplegic arrest and 60 min of reperfusion. In the control group, the hearts were perfused with a crystalloid cardioplegic solution (CPS) through the aortic root every 20 min during arrest. In the treated group, the hearts received CPS containing puerarin (2 mg/kg). Cardiac hemodynamic variables were monitored throughout the experiments. Left ventricular function curves were formed before ischemia and after 60 min of reperfusion. The results showed that the recovery of left ventricular function in the treated group was significantly better than that in the controls (81 +/- 11% versus 39 +/- 7%, P less than 0.01). Compared with preischemic values, the increase of coronary blood flow (CBF) at cardiac arrest in the puerarin-treated group was higher than that in the control group (214 +/- 11 versus 177 +/- 4 ml/min, P less than 0.01). The data indicate that puerarin has protective effects on the cardiac function after prolonged arrest and reperfusion.

Animals↗
PubMed2002

Gender-specific responses of lean body composition and non-gender-specific cardiac function improvement after GH replacement in GH-deficient adults.

GH deficiency (GHD) in adulthood is accompanied by physical and psychological impairments. One hundred fifteen patients (67 male, 48 female) with pronounced GHD were enrolled in a randomized, double-blind, placebo-controlled study with objectives that included effects on body composition, cardiac structure, and function and safety of replacement therapy with recombinant human GH (Saizen). Sixty patients (31 male, 29 female) received GH at a dose of 0.005-0.010 mg/kg.d, and 55 patients (36 male, 19 female) received placebo for 6 months. Assessment of body composition by dual-energy x-ray absorptiometry demonstrated a treatment difference in lean body mass increase of 2.1 kg (between-group comparison, P < 0.0001), which was significantly greater among males than females (P < 0.0001) [males: GH, +3.13 kg (2.42, 3.84); placebo, +0.11 kg (-0.60, 0.82); and females: GH, +0.64 kg (-0.15, 1.44); placebo: -0.90 kg (-2.20, 0.39)] [mean change 0-6 months (95% confidence limits)] and was associated with IGF-I changes. The decrease in fat mass of 2.8 kg (between-group comparison, P < 0.0001) noted by DEXA was also evident from bioelectric impedance and anthropometric measurements. Echocardiography showed comparable improvement in left ventricular systolic function after GH treatment in both genders. End-systolic volume decreased by 4.3 +/- 10.5 ml (from 35.8 +/- 17.6 ml; between-group comparison, P = 0.035) and ejection fraction increased by 5.1 +/- 10.0% (from 55.0 +/- 11.2%; between-group comparison, P = 0.048), approaching normalcy. Diastolic function did not change as assessed by isovolumic relaxation time, early diastolic flow, diastolic flow secondary to atrial contraction, or ratio of peak mitral early diastolic and atrial contraction velocity. GH treatment was well tolerated, with adverse events primarily related to effects on fluid balance. No apparent relationship between IGF-I levels and the occurrence or severity of adverse events was identified. In conclusion, GH replacement therapy in adults with GHD demonstrated beneficial effects on lean body mass composition that was more pronounced in males than females. In contrast, cardiac function improvement appears to benefit both genders equally.

Adult↗
PubMed2001

Tissue engineering of functional cardiac muscle: molecular, structural, and electrophysiological studies.

The primary aim of this study was to relate molecular and structural properties of in vitro reconstructed cardiac muscle with its electrophysiological function using an in vitro model system based on neonatal rat cardiac myocytes, three-dimensional polymeric scaffolds, and bioreactors. After 1 wk of cultivation, we found that engineered cardiac muscle contained a 120- to 160-microm-thick peripheral region with cardiac myocytes that were electrically connected through gap junctions and sustained macroscopically continuous impulse propagation over a distance of 5 mm. Molecular, structural, and electrophysiological properties were found to be interrelated and depended on specific model system parameters such as the tissue culture substrate, bioreactor, and culture medium. Native tissue and the best experimental group (engineered cardiac muscle cultivated using laminin-coated scaffolds, rotating bioreactors, and low-serum medium) were comparable with respect to the conduction velocity of propagated electrical impulses and spatial distribution of connexin43. Furthermore, the structural and electrophysiological properties of the engineered cardiac muscle, such as cellularity, conduction velocity, maximum signal amplitude, capture rate, and excitation threshold, were significantly improved compared with our previous studies.

Animals↗
PubMed1977

Cardiac function, coronary flow and MVO2 in hypertrophy induced by pressure and volume overloading.

Myocardial function, flow and O2 consumption were compared in cardiac hypertrophy induced by pressure-loading (P) and by volume overloading (V). Increases in LV-to-body weight ratios in P and V hypertrophied hearts were comparable. Indices of LV function such as cardiac output, stroke volume, stroke work, minute work, peak LV dP/dt, ratio of peak LV dP/dt-to-isovolumic pressure and -to-LVEDP, and Vmax were significantly reduced from normal only in hypertrophy induced by V. Left ventricular coronary flow was reduced from 167.1 +/- 27.2 in normal dogs to 146.2 +/- 17.1 cm3/min-100 g-1 in P hypertrophy, and was reduced further to 82.5 +/- 8.2 cm3/min-100 g-1 in V hypertrophy. Flows decreased similarly in epicardium and endocardium in both hypertrophied hearts. Cardiac O2 extraction in P and V hearts was greater than in control hearts. Myocardial O2 consumption was maintained at control values in P hypertrophy, and decreased by 54 +/- 3% in V hypertrophy. These findings indicate that LV function is impaired at rest in hypertrophy induced by V and is normal in hypertrophy induced by P.

Animals↗
PubMed1997

Growth hormone attenuates early left ventricular remodeling and improves cardiac function in rats with large myocardial infarction.

OBJECTIVES: We sought to investigate the cardiac effects of growth hormone (GH) administration during the early phase of pathologic remodeling in a rat model of large myocardial infarction (MI). BACKGROUND: Recent evidence suggests that exogenous administration of GH evokes a hypertrophic response and increases left ventricular (LV) function in vivo in rats with normal or chronically failing hearts. We hypothesized that these effects would attenuate ventricular remodeling early after MI. METHODS: Fifty-eight male rats underwent sham operation (n = 19) or had induced MI (n = 39). The day after the operation, the infarcted rats were randomized to receive 3 weeks of treatment with GH, 3 mg/kg body weight per day (n = 19) or placebo (n = 20). Echocardiography, catheterization and isolated whole heart preparations were used to define cardiac structure and function. RESULTS: Growth hormone caused hypertrophy of the noninfarcted myocardium in a concentric pattern, as noted by higher echocardiographic relative wall thickness at 3 weeks and by morphometric histologic examination. Left ventricular dilation was reduced in the GH-treated versus placebo group (echocardiographic LV diastolic diameter to body weight ratio 2.9 +/- 0.1 vs. 3.5 +/- 0.2 cm/kg; p < 0.05). In vivo and in vitro cardiac function was improved after GH treatment. Despite elevated insulin-like growth factor-1 (IGF-1) serum levels in GH-treated rats, myocardial IGF-I messenger ribonucleic acid was not different among the three groups, suggesting that an increase in its local expression does not appear necessary to yield the observed effects. CONCLUSIONS: These data demonstrate that early treatment of large MI with GH attenuates the early pathologic LV remodeling and improves LV function.

Animals↗
PubMed2004

Maternal hyperglycemia improves fetal cardiac function during tachycardia-induced heart failure in pigs.

BACKGROUND: Fetal tachycardia often leads to cardiac failure, which in experimental settings can be prevented by direct fetal glucose-insulin administration. In this study, we hypothesize that similar effects can be obtained indirectly by inducing maternal hyperglycemia. METHODS AND RESULTS: Systolic and diastolic indices (dP/dt(max) and tau) of left ventricular function were measured by use of high-fidelity catheters during 180 minutes of aggressive atrial pacing ( approximately 300 bpm) in 12 preterm porcine fetuses. In 6 fetuses, maternal hyperglycemia (15 mmol/L) was induced for the last 120 minutes of pacing. The remaining fetuses served as controls. Glucose, insulin, and free fatty acid levels were determined, as was fetal myocardial glycogen content. Maternal glucose infusion led to significant fetal hyperglycemia and hyperinsulinemia but did not change the inherently low fetal levels of free fatty acids. There were no differences between groups with regard to dP/dt(max) (1025+/-226 and 1037+/-207 mm Hg, P=NS) and tau (20.6+/-2.0 and 21.4+/-1.6 ms, P=NS) at baseline (100%). During the 180 minutes of pacing, systolic function (dP/dt(max)) and diastolic function (tau) deteriorated more in the control group than in the hyperglycemic group (P<0.001 for both). At 180 minutes, dP/dt(max) was 62+/-18% of baseline in controls and 85+/-11% in hyperglycemic fetuses (P=0.03), and tau was 117+/-12% and 98+/-4%, respectively (P=0.004). CONCLUSIONS: Induced maternal hyperglycemia improves fetal cardiac function during fetal tachycardia and suggests a possible additional therapeutic option to improve the function of the failing fetal heart before or during antiarrhythmic therapy. The findings may be relevant in fetal heart failure in general.

Animals↗
PubMed1980

Cardiac function in patients with prior myocarditis.

Gated cardiac blood-pool imaging under rest and exercise was used to assess left-ventricular functional reserve in six asymptomatic patients with prior myocarditis and six age matched control subjects. Coronary artery disease was excluded in three of the six patients by coronary arteriography. In the remaining three, coronary artery disease was thought unlikely on the basis of history and the presence, during exercise, of a normal ECG and normal Tl-201 myocardial image. Conventional indices of resting left-ventricular function--including cardiothoracic ratio, echocardiographic left-ventricular diameter, and percentage change in minor diameter--were normal in those with prior myocarditis. The mean resting left-ventricular ejection fraction was also normal by gated blood-pool imaging, and not significantly different from that for control patients: 0.58 +/- 0.05 and 0.65 +/- 0.02, respectively. Three patients with prior myocarditis had resting left-ventricular ejection fractions of less than 0.50. On exercise, the patients with prior myocarditis decreased their mean left-ventricular ejection fraction by an average of 8% compared with an increase of 15% in the control group (p less than 0.01). This study suggests that asymptomatic patients with prior myocarditis have left-ventricular dysfunction that may not be clinically apparent, and suggests the need for further long-term follow-up.

Adult↗
PubMed2004

Comparison of systolic cardiac function before and after treatment of atrial fibrillation in horses with and without additional cardiac valve insufficiencies.

Clinical, electrocardiographic and echocardiographic examinations were conducted before therapy and 4 days after conversion to normal sinus rhythm in 15 horses with a history of atrial fibrillation of 2-6 months duration. Seven horses showed no other signs of cardiac disease. Four horses suffered additionally from mitral valve insufficiency, while six horses had aortic valve insufficiency, including two of the four horses with mitral valve insufficiency, but none had signs of congestive heart failure. Doppler echocardiographic estimates of various variables were made for assessment of systolic heart function. These included heart rate, stroke volume, cardiac output and cardiac output per kg of body weight (heart index). After conversion to normal sinus rhythm, the horses without heart valve insufficiency showed a statistically significantly decreased heart rate (-24%) and cardiac output (-3%), but an increase in stroke volume (+8.4%) and heart index (+9%). The horses with heart valve insufficiency experienced a statistically significant decrease in heart rate (-21%) after conversion to normal sinus rhythm, but showed an increase in all other variables. Cardiac output increased statistically significantly by 20%, stroke volume by 54% and heart index by 58%.

Animals↗
PubMed1971

Experimental myocardial infarction. 8. Chronotropic augmentation of cardiac function in left ventricular failure of acute and healing stages in intact conscious dogs.

The hemodynamic effects of tachycardia induced by atrial pacing were investigated in left ventricular failure of acute and healing experimental myocardial infarction in 20 intact, conscious dogs. Myocardial infarction was produced by gradual inflation of a balloon cuff device implanted around the left anterior descending coronary artery 10-15 days prior to the study. 1 hr after acute myocardial infarction, atrial pacing at a rate of 180 beats/min decreased left ventricular end-diastolic pressure from 19 to 8 mm Hg and left atrial pressure from 17 to 12 mm Hg, without change in cardiac output. In the healing phase of myocardial infarction 1 wk later, atrial pacing decreased left ventricular end-diastolic pressure from 17 to 9 mm Hg and increased the cardiac output by 37%. This was accompanied by evidence of peripheral vasodilation. In two dogs with healing anterior wall myocardial infarction, left ventricular failure was enhanced by partial occlusion of the circumflex coronary artery. Both the dogs developed pulmonary edema. Pacing improved left ventricular performance and relieved pulmonary edema in both animals. In six animals propranolol was given after acute infarction, and left ventricular function deteriorated further. However the pacing-induced augmentation of cardiac function was unaltered and, hence, is not mediated by sympathetics.The results show that the spontaneous heart rate in left ventricular failure of experimental canine myocardial infarction may be less than optimal and that maximal cardiac function may be achieved at higher heart rates.

Adrenergic beta-Antagonists↗
PubMed1993

Effects of the single and repeated administration of benazepril on systemic and forearm circulation and cardiac function in hypertensive patients.

The hemodynamic and cardiac effects of the new angiotensin-converting enzyme inhibitor, benazepril, were studied in 28 hypertensives in a double blind, placebo-controlled, between-patient study. Hemodynamic studies were performed noninvasively by means of M-mode echo (central hemodynamics and left ventricular systolic function), 2-D echo-Doppler (left ventricular diastolic function), and pulsed Doppler flowmetry (forearm circulation). Examinations were done at the end of a placebo run-in period and 3 hours after benazepril administration, both on the first day and after 6 weeks of treatment (10 or 20 mg once daily, according to patient response). In comparison with placebo, benazepril reduced systolic (p = 0.04) and diastolic (p = 0.003) blood pressure, because of a significant reduction in systemic vascular resistance (p = 0.03), while cardiac output was unchanged. Forearm vascular resistance was reduced and brachial artery compliance increased, although not to a statistically significant level (both p = 0.07). Both systolic and diastolic left ventricular function were positively influenced by the afterload reduction: End-systolic stress was reduced by 12% (p = 0.07), as was the late diastolic peak flow velocity (p = 0.02). All hemodynamic changes were evident after acute benazepril administration, and no differences was observed between acute and repeated treatment. We conclude that, similar to other ACE-inhibitors, benazepril reduces blood pressure through a reduction in vascular resistance, while cardiac output and heart rate are unaffected. These hemodynamic effects occur as early as after the first administration and exert a favorable influence on left ventricular dynamics.

Adult↗
PubMed1986

Effects of nifedipine on hemodynamics and cardiac function in patients with normal left ventricular ejection fraction already treated with propranolol.

The interaction between nifedipine and propranolol on cardiac hemodynamics and function was investigated in 9 patients with normal left ventricular (LV) function who were undergoing cardiac catheterization for complaints of chest pain. Only 2 patients had angiographic evidence of significant coronary artery disease but no patient had clinical evidence of ischemia during the study. All patients were pre-treated with propranolol, 30 to 320 mg/day (mean +/- standard deviation 210 +/- 122); the propranolol serum level ranged from 43 to 246 ng/ml (mean 203 +/- 62). The administration of nifedipine resulted in a decrease in blood pressure (from 94 +/- 11 to 85 +/- 13 mm Hg, p less than 0.05), increase in heart rate (from 59 +/- 6 to 65 +/- 7 beats/min, p less than 0.05), and an increase in both mean right atrial and mean pulmonary artery wedge pressures (from 8 +/- 3 to 9 +/- 3 mm Hg and from 13 +/- 3 to 14 +/- 4 mm Hg, respectively, both p less than 0.05). Cardiac index increased (from 2.3 +/- 0.3 to 2.7 +/- 0.2 liters/min/m2, p less than 0.01). Stroke volume index also increased significantly (from 39 +/- 5 to 43 +/- 6 ml/m2) and systemic vascular resistance decreased (from 1,715 +/- 369 to 1,255 +/- 271 dynes s cm-5, p less than 0.01). No significant change was noted in pulmonary vascular resistance (148 +/- 94 vs 140 +/- 62 dynes s cm-5), LV stroke work index (44 +/- 9 vs 42 +/- 10 g-m/m2), LV end-diastolic pressure (15 +/- 2 vs 16 +/- 2 mm Hg).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2002

Echocardiographic assessment of cardiac function in diabetic db/db and transgenic db/db-hGLUT4 mice.

Control db/+ and diabetic db/db mice at 6 and 12 wk of age were subjected to echocardiography to determine whether contractile function was reduced in vivo and restored in transgenic db/db-human glucose transporter 4 (hGLUT4) mice (12 wk old) in which cardiac metabolism has been normalized. Systolic function was unchanged in 6-wk-old db/db mice, but fractional shortening and velocity of circumferential fiber shortening were reduced in 12-wk-old db/db mice (43.8 +/- 2.1% and 8.3 +/- 0.5 circs/s, respectively) relative to db/+ control mice (59.5 +/- 2.3% and 11.8 +/- 0.4 circs/s, respectively). Doppler flow measurements were unchanged in 6-wk-old db/db mice. The ratio of E and A transmitral flows was reduced from 3.56 +/- 0.29 in db/+ mice to 2.40 +/- 0.20 in 12-wk-old db/db mice, indicating diastolic dysfunction. Thus a diabetic cardiomyopathy with systolic and diastolic dysfunction was evident in 12-wk-old diabetic db/db mice. Cardiac function was normalized in transgenic db/db-hGLUT4 mice, indicating that altered cardiac metabolism can produce contractile dysfunction in diabetic db/db hearts.

Animals↗