Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Cardiac function”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,225 records · Page 68Linked to original sources
PubMed1996

Relationships of cardiac function and structure to blood pressure rhythms.

It is well known that hemodynamic load is one of the most important determinants of cardiac structure and function. Circadian variations in blood pressure (BP) values are usually accompanied by consensual changes in peripheral resistance and/or cardiac output. In recent years, in hypertensive patients with left ventricular hypertrophy (LVH), a reduction in the circadian variations of BP and, in particular, a lack of nocturnal decline were observed; patients with only a small reduction in BP or none at all during the night were considered "non-dippers." In patients in whom a regression of LVH was obtained after prolonged antihypertensive therapy, restoration of the circadian rhythm of BP was also observed. However, the division of patients into "dippers" and "non-dippers" is arbitrary and poorly standardized and repeatable, and in the recent SAMPLE study, most hypertensive patients with LVH were dippers. Therefore, we should be particularly cautious about the conclusions drawn using this index. On the other hand, in patients with LVH, reduced activity of the low pressure cardiopulmonary baroreceptors and impaired day-to-night modulation of autonomic nervous system activity were observed. Therefore, cardiac structural alterations may possibly impair BP modulation; on the other hand, the opposite could also be true: a primarily altered BP modulation, through a persistently elevated afterload, could increase cardiac mass. Therefore, the interrelationships between cardiac structure and BP modulation are complex, and as a result, new and more specific methods of evaluation circadian changes in BP are needed to better clarify their reciprocal influences.

Blood Pressure↗
PubMed1998

Assessment of pulmonary and cardiac function after high dose chemotherapy with BEAM and peripheral blood progenitor cell transplantation.

BACKGROUND: Limited information is available regarding the cardiac and pulmonary effects of high dose chemotherapy (HDCT) and autologous peripheral blood progenitor cell (PBPC) transplantation. METHODS: The authors evaluated cardiac and pulmonary function after BEAM (BCNU 300 mg/m2, etoposide 400 mg/m2/day x 3 days, cytosine arabinoside 200 mg/m2/day x 4 days, and melphalan 140 mg/m2), HDCT, and PBPC transplantation in 26 patients with non-Hodgkin's lymphoma or Hodgkin's disease. Therapy prior to BEAM included doxorubicin (25 patients), bleomycin (6 patients), and mediastinal irradiation (4 patients). All patients had pulmonary function tests (PFTs) and equilibrium radionuclide angiography before and at a median of 57 weeks after transplantation. RESULTS: Prior to high dose therapy, 8 patients had abnormal PFTs, including 6 with a diffusing capacity of the lung for carbon monoxide (DLCO) <70% of predicted value. At the time of reevaluation after HDCT, all patients included in the study were in complete remission, and none had received additional therapy after transplantation. At a median of 77 weeks after transplantation, none of the patients had cardiac or pulmonary symptoms. Moreover, there were no significant changes in total lung capacity, forced vital capacity, forced expiratory volume in 1 second/forced vital capacity, DLCO, or left ventricular ejection fraction values when compared with baseline studies. CONCLUSIONS: The authors concluded that HDCT with BEAM and PBPC transplantation did not result in significant cardiac or pulmonary toxicity, even in patients with borderline pretransplantation PFT values. Further studies of patients undergoing HDCT and PBPC transplantation are needed.

Adult↗
PubMed1985

Effects of 1-O-alkyl-2-acetyl-sn-glycero-3-phosphocholine (platelet activating factor) on cardiac function in perfused guinea-pig heart.

The direct cardiac action of 1-O-alkyl-2-acetyl-sn-glycero-3-phosphocholine (PAF) was studied in isolated perfused guinea-pig heart preparations. PAF produced a fall in left ventricular pressure, decreases in the rate of rise of the left ventricular pressure (dp/dt) and coronary flow, but had no effect on heart rate. These results indicate that PAF is a cardiodepressant with inotropic selectivity and this effect on heart is blocked by CV-3988, a specific PAF antagonist.

Animals↗
PubMed2001

Intracoronary infusion of skeletal myoblasts improves cardiac function in doxorubicin-induced heart failure.

BACKGROUND: Skeletal myoblast transplantation is promising for the treatment of end-stage heart failure. Direct intramyocardial injection is useful for local cell delivery but may not be effective in global dissemination of cells into the heart, which would be advantageous in treating generalized cardiac dysfunction as in dilated cardiomyopathy. We hypothesized that intracoronary infusion of myoblasts would disseminate cells more effectively, leading to functional improvement in global heart failure. METHODS AND RESULTS: Heart failure was induced by the intraperitoneal administration of doxorubicin (total dose 15 mg/kg) in rat. One million primary skeletal myoblasts were then infused via the coronary arteries of an excised, failing doxorubicin-treated heart. After incubation under increased intracoronary pressure, the hearts were subsequently transplanted into syngeneic recipients. For the control group, doxorubicin-treated hearts were infused with medium only and transplanted. Four weeks after transplantation, Langendorff perfusion demonstrated that both maximum dP/dt (2797.6+/-103.3 versus 2326.9+/-133.1 mm Hg/s, P=0.01) and minimum dP/dt (-2067.4+/-88.1 versus -1718.8+/-91.3 mm Hg/s, P=0.02) were improved in myoblast-transplanted hearts compared with medium-infused hearts. This was associated with a sharper slope of the left ventricular developed pressure-volume curve and a reduced slope of the end-diastolic pressure-volume relation in the myoblast-transplanted hearts. Immunohistochemistry for skeletal myosin heavy chain showed that globally disseminated myoblasts had survived and differentiated into multinucleated myotubes that had aligned with the cardiac fiber axis within host myocardium. No significant myocardial infarction was observed. CONCLUSIONS: We demonstrated the feasibility and efficiency of skeletal myoblast transplantation via the intracoronary route as a promising strategy for improving cardiac function in global heart failure.

Animals↗
PubMed2005

Cardiac function in children post-orthotopic liver transplantation: echocardiographic parameters and biochemical markers of subclinical cardiovascular damage.

Tacrolimus and cyclosporin A (CsA), the mainstay of preventive therapy for solid organ rejection, may cause various side-effects, such as hypertension and nephrotoxicity. Furthermore, tacrolimus is associated with cardiac hypertrophy. In the immediate post-transplant period, both drugs raise the levels of Endothelin-1 (ET), a potent vasoconstrictor; and of B-type Natriuretic Peptide (BNP), a sensitive marker of left ventricular volume overload, which may precede echocardiographic changes of cardiac dysfunction. The aim of the study was to investigate the presence of cardiac damage, by echocardiography and by the biochemical markers BNP and ET, in post-orthotopic liver transplantation (OLT) children, receiving long-term immunosuppressive therapy. ET (ELISA) and BNP (RIA) were measured in plasma of 18 children, post-OLT and 18 healthy controls. Children post-OLT were echocardiographically assessed for left ventricular mass (interventricular septum and posterior wall dimensions), systolic function (ejection fraction, fractional shortening) and diastolic parameters (mitral valve E and A waves, deceleration time, isovolumic relaxation time). None of the post-transplant recipients had a history or physical examination consistent with cardiac disease and all recipients were normotensive. Echocardiography revealed no systolic or diastolic dysfunction in any of the recipients. The mean ET and BNP levels tended to be higher among children post-liver transplant, compared with healthy controls (ET: 4.22 +/- 5.35 pg/mL vs. 2.1 +/- 2.0 pg/mL; BNP: 7.05 +/- 4.4 pg/mL vs. 5.87 +/- 2.0 pg/mL, respectively, mean +/- s.d.) although differences did not reach statistical significance. Three children (17%) had elevated BNP and/or ET levels. A strong correlation was observed between ET and BNP levels in post-OLT children (r = 0.79, p < or = 0.05). No correlation was found between ET or BNP levels and echocardiographic findings. In children receiving long-term immunosuppressive therapy post-OLT, although cardiac function is grossly preserved, ET and BNP levels tend to be higher than in healthy, age-matched children. Thus, elevated levels of BNP and/or ET may identify patients with early cardiac damage.

Adolescent↗
PubMed1998

Effect of vesnarinone on cardiac function in patients with severe congestive heart failure.

BACKGROUND: Vesnarinone has yielded controversial results on morbidity in patients with congestive heart failure. We tested the hypothesis that vesnarinone may have a beneficial effect on cardiac remodeling and function. METHODS: Thirty-four patients with left ventricular ejection fraction (LVEF) <30% (17 treated with vesnarinone) underwent an echocardiography at baseline and at 12+/-5 months. Left ventricular end-diastolic and end-systolic volume, mitral regurgitation, diastolic filling, and right ventricular area change were quantified and compared. RESULTS: When the vesnarinone group was considered as a whole, there was no significant effect of vesnarinone on cardiac systolic and diastolic function or remodeling. However, an increase in LVEF >7% was observed in six of the vesnarinone patients and none of the control group. Vesnarinone improved right and left ventricular systolic function significantly in patients with initial LVEF <25%. CONCLUSIONS: In severe congestive heart failure, vesnarinone induces variable responses but improves biventricular performance in patients with the most impaired initial function.

Aged↗
PubMed1992

Quantitative ultrasonic imaging: tissue characterization and instantaneous quantification of cardiac function.

Quantitative myocardial tissue characterization is being developed to complement and expand conventional echocardiography by delineating the physical state of myocardium under diverse pathophysiologic conditions. Real-time quantitative integrated backscatter imaging has already been applied to patients with ischemic heart disease, hypertrophic cardiomyopathy, and cardiac allograft rejection in clinical investigations performed in the United States, Europe, and Japan. A recently introduced modification of imaging processing algorithms employed for characterization of tissue facilitates automatic detection of endocardial-blood interfaces and on-line quantification of ventricular size and function. Further progress and anticipated developments in quantitative ultrasonic imaging will undoubtedly augment the clinical applications of tissue characterizations based on myocardial integrated backscatter for improved diagnosis, elucidation of pathophysiology, and assessment of cardiac function.

Animals↗
PubMed2005

Nitric oxide donors alter cardiomyocyte cytokine secretion and cardiac function.

OBJECTS: The mechanisms by which nitric oxide produces beneficial/detrimental effects on physiologic function are unclear. In this study, we hypothesized that nitric oxide promotes cyclic guanosine monophosphate (cGMP) formation, which, in turn, promotes cardiomyocyte secretion of inflammatory cytokines as well as accumulation of intracellular Na+/Ca2+; these factors contribute to altered cardiac contractile function. DESIGN: Laboratory study. SETTING: Medical Center. SUBJECTS: Adult Sprague Dawley rats weighing 325-350 g. INTERVENTIONS: Cardiomyocytes were prepared by collagenase perfusion of rat hearts; cells were plated (5 x 10(4) cells/microtiter well) and challenged with either vehicle or nitric oxide donor (S-nitroso-N-acetyl-penicillamine [SNAP] or PAPA NONOATE, 3-[2-Hydroxy-2-nitroso-1-propythdrazinol]-1-propanamine], NOC-15 [PAPA-NO], 0.3 or 1.0 mM of each nitric oxide donor) in the presence/absence of methylene blue (10 microM/L to inhibit cGMP). After 3 hrs, supernatants were collected to measure nitrite/nitrate (nitric oxide), cytokines (tumor necrosis factor-alpha, interleukin-1beta, interleukin-6), and cGMP levels; cells were then loaded with a fluorescent indicator (Fura-2AM or sodium-binding benzofurzan isophthalate) to measure myocyte Ca2+ or Na+, respectively. Parallel experiments included the addition of nitric oxide donor (0.3 or 1.0 mM SNAP or PAPA-NO) to perfused hearts in presence or absence of the methylene blue to examine cGMP-mediated effects on myocardial contraction-relaxation, while other experiments determined a) potential lipopolysaccharide contamination of myocyte preparations; and b) whether a cGMP analogue recapitulated the effects of nitric oxide donors on cytokine secretion. MEASUREMENTS AND MAIN RESULTS: Nitric oxide donors produced a dose-dependent increase in cGMP levels in myocyte supernatants as well as an increase in myocyte cytokine secretion, increased myocyte loading of Na+/Ca2+, and produced myocardial contractile dysfunction. Addition of the cGMP analog, 8-bromo-cGMP, recapitulated the effects of nitric oxide donors on myocyte cytokine secretion. Nitric oxide donor-related effects were ablated by pretreatment of myocytes or isolated hearts with methylene blue. Treatment of myocytes with recombinant bactericidal/permeability-increasing protein to scavenge lipopolysaccharide confirmed that cytokine responses to nitric oxide donors were not related to lipopolysaccharide contamination of myocyte preparations. CONCLUSIONS: We suggest that nitric oxide synthesis in injury and disease promotes cGMP formation, which, in turn, modulates cardiac contraction/relaxation by a) altering cardiomyocyte secretion of inflammatory cytokines and b) altering myocyte handling of Na+/Ca2+.

Animals↗
PubMed2001

The effect of kidney transplant on cardiac function: an echocardiographic perspective.

Kidney transplant (KT) resolves many of the cardiac abnormalities associated with chronic kidney failure (CKF). This study analyzed cardiac alterations of kidney failure and their modification with transplant. Thirteen patients in CKF underwent conventional echocardiograms, dobutamine stress echocardiograms, and injection of contrast to examine perfusion before KT and 3 months after transplant. Nine patients had evidence of left ventricular hypertrophy and six had evidence of diastolic dysfunction. Wall thickness, left ventricular mass, and mass index diminished after KT; only two patients continued to manifest hypertrophy. Left ventricular systolic diameters and volumes diminished at 3 months, and diastolic diameters after 4 months. Left ventricular fractional shortening and ejection fraction increased 3 months after transplant. At the end of the study, only two patients continued to show diastolic dysfunction. Dobutamine echocardiograms showed no segmental wall-movement abnormalities. Myocardial perfusion was normal before and after transplant. The results suggest that KT diminishes hypertrophy and improves left ventricular systolic and diastolic function. Echocardiography provides valuable information for detection and follow-up of cardiac abnormalities in patients with kidney disease. Evaluation of segmental wall movement and myocardial perfusion aid in demonstrating that our studied patients with CKF had no indirect signs of coronary artery disease.

Adult↗
PubMed1987

Cardiac function as related to adrenergic activity in hypertensive left ventricular hypertrophy.

Studies in experimental animals and in hypertensive patients have shown that changes in cardiac anatomy and function are not just a simple consequence of the increased pressure load. The activity of the sympathetic nervous system is one of the factors that may influence cardiac performance and also, possibly, the cardiac anatomy of hypertensive patients. Animal studies have strongly suggested a possible role of adrenergic factors in the development of left ventricular hypertrophy. In man, plasma catecholamines are usually higher in hypertensive patients with left ventricular hypertrophy, and a correlation between left ventricular mass and plasma noradrenaline has also been observed. The decrease of cardiac performance after acute beta blockade has been found to be directly related to basal plasma noradrenaline concentration. An impaired response to beta-adrenergic stimulation has been reported in hypertensive animals and has been confirmed in hypertensive patients with left ventricular hypertrophy.

Adult↗
PubMed2006

Inhibition of cyclooxygenase-2 improves cardiac function following long-term preservation.

BACKGROUND: Cyclooxygenase (COX) is an intracellular enzyme that converts arachidonic acid to prostaglandin endoperoxide (PGG(2)). There are two isoforms of COX, namely constitutive COX-1 and inducible COX-2. It has been reported that COX-2 plays an important role in ischemia-reperfusion injury and that COX-2 mRNA and protein expression were up-regulated during cardiac allograft rejection. FK3311 is a suppressor of COX-2 activation. The purpose of this study was to evaluate the effectiveness of inhibiting COX-2 with FK3311 for the minimization of ischemia-reperfusion injury and for the improvement of donor heart function following transplantation in a canine model. MATERIALS AND METHODS: Adult mongrel dogs were used. After the measurement of hemodynamic parameters [cardiac output (CO), left ventricular pressure (LVP), and the maximum rates of increase and decrease in LVP (+/-LVdp/dt)], coronary vascular beds were washed out with a hypothermic (4 degrees C) University of Wisconsin (UW) solution following cardiac arrest in response to cold (4 degrees C) glucose-insulin-potassium solution. The heart was then excised and preserved in hypothermic (4 degrees C) UW solution for 12 h. FK3311 (3 mg/kg) was administered intravenously to five dogs prior to reperfusion, while vehicle was administered intravenously to a control group (n = 5). After 3 h of orthotopic transplantation using cardiopulmonary bypass, the hemodynamic parameters were compared with preoperative values of the donor animals under the condition of 10 mm Hg right atrial pressure and 5 mug/kg/min dopamine support. RESULTS: The recovery rates of CO and +/-LVdP/dt were significantly (P < 0.05) higher in the FK-treated dogs than in the controls (CO: 93 +/- 6 versus 66% +/- 4%; +LVdp/dt: 125 +/- 8 versus 77 +/- 10%; and -LVdp/dt: 81 +/- 7 versus 52 +/- 6%; for FK-treated versus control dogs, respectively). The recovery rate of LVP was higher in the FK-treated dogs than in the controls (90 +/- 5 versus 72 +/- 5%), but this difference was not statistically significant. Immunohistochemical staining revealed that COX-2 expression was reduced significantly in the myocardium of FK-treated dogs compared with controls. CONCLUSION: Hemodynamic parameters following transplantation were improved significantly in dogs treated with FK3311. Therefore, the inhibition of COX-2 improves transplanted cardiac function following long-term preservation.

Adenosine↗
PubMed1998

Evaluation of cardiac status in iron-loaded thalassaemia patients following bone marrow transplantation: improvement in cardiac function during reduction in body iron burden.

Iron-induced cardiac disease is the primary cause of death in transfused patients with thalassaemia major. The beneficial effects of deferoxamine mesylate on clinical cardiac disease have been well described but the impact of therapy on subclinical cardiac dysfunction is unknown. To assess the reversibility of subclinical cardiac dysfunction we studied the cardiac status during iron depletion treatment (phlebotomy) in iron overloaded patients, cured of thalassaemia by marrow transplantation, without clinical manifestation of heart failure but with alteration in both left ventricular diastolic function and in contractility property. 32 patients were studied and demonstrated a slight but significant impairment in the morphology and function if compared with matched normal controls. 17 of these patients were submitted to sequential echocardiographic evaluations during the phlebotomy programme. Following completion of the programme, normalization of the indices of contractility and normalization of diastolic function were observed. This study indicates that transplanted thalassaemia patients with subclinical left ventricular diastolic dysfunction and impaired left ventricular contractility may reverse these processes with an effective regimen of iron reduction such as phlebotomy.

Adolescent↗
PubMed1985

[Effects of prostacyclin on the cardiac functions and energy metabolism in the perfused rat heart].

Recently, prostacyclin (PGI2) has been reported to have a role of potential importance in myocardial ischemia. The direct effects of PGI2 on ischemic myocardial injury (60 minutes ischemia at 30 degrees C) were examined, using a hemoglobin free isolated rat heart perfused by the Langendorff's technique. Dual-wavelength reflectance spectrophotometry was used to measure myoglobin oxygenation in cardiac tissue, from which the intracellular oxygen concentration was calculated. The effect of PGI2 on cardial function under normoxic perfusion condition was studied. PGI2 was infused for 10 minutes with the doses of 5ng/g X body weight per minute. PGI2 infusion increased heart rate, LV dp/dt and myocardial oxygen consumption. The average 9.7% increase in myoglobin oxygenation was noted during PGI2 infusion which indicated the improvement in tissue oxygen metabolism. The global ischemia was produced for 60 minutes at 30 degrees C, following to the pretreatment of 10 minutes infusion of PGI2, by the discontinuation of Langendorff's perfusion. Recovery of cardiac function such as double product and LV dp/dt at 15 minutes after reperfusion was significantly higher in the PGI2 treated group than in hearts receiving only the vehicle. Infusion of PGI2 inhibited the decrease in ATP level of the ischemic myocardium at 15 minutes after reperfusion (P less than 0.025, P less than 0.05). PGI2 prevented the increase in lactate release from the ischemic myocardium, observed in vehicle group at 1 minutes after reperfusion. In summary, prostacyclin seems to have a direct cytoprotective effect on ischemic myocardium.

Animals↗
PubMed1984

Noninvasive determination of exercise cardiac function following Fontan operation.

The purpose of this investigation was to define mechanisms which increase cardiac output during exercise in patients without a functioning right ventricle. Radionuclide studies were performed at rest and during upright bicycle exercise on 16 patients following Fontan procedures and compared to studies in 10 normal children. The mean cardiac index of patients following Fontan procedures was 5.2 +/- 2.0 L/min/m2 (standard deviation) at rest and increased to 9.4 +/- 3.5 L/min/m2 during exercise (p less than 0.0001). Exercise values were similar to those observed in normal children. The mechanisms utilized to achieve high cardiac output following Fontan procedures included an increase in heart rate. Mean systemic ventricular ejection fractions were significantly less than in normal children. The resting ventricular end-diastolic volume and stroke volume indices were above normal and remained constant during exercise to high heart rates. These data clearly document that a large exercise cardiac output can be achieved by patients without a functioning right ventricle.

Adolescent↗
PubMed2003

The effect of maternal cocaine exposure on neonatal rat cardiac function.

Fetal cocaine exposure has been associated with a variety of cardiovascular dysfunctions in humans. We treated pregnant rats with either saline or cocaine at 60 mg/kg by gastric lavage for the entire gestational period and for 14 days after parturition. We then performed high-frequency transthoracic echocardiography to determine whether cocaine exposure affected neonatal cardiac contractile function in vivo in 7- and 14-day-old neonatal rats. All studies were performed in the unsedated, conscious state. Heart rate (HR) and systolic function, expressed as fractional area of change at the midpapillary muscle level, were calculated from two-dimensional images. Resting HR was faster in the cocaine-exposed group at both ages, but baseline contractile function was not different between control (CTL) and cocaine-exposed (COC) neonatal rats. Dobutamine induced a significant increase in HR in all groups at only the largest dose tested (Day 7 CTL HR increased from 438 +/- 3 bpm to 462 +/- 10 bpm; Day 7 COC HR increased from 466 +/- 3 bpm to 493 +/- 7 bpm; Day 14 CTL HR increased from 443 +/- 4 bpm to 487 +/- 4 bpm; Day 14 COC HR increased from 477 +/- 4 bpm to 501 +/- 5 bpm). Dobutamine elicited a significant increase in contractile response at both Day 7 (from 76.6% +/- 0.6% to 81.5% +/- 0.7%) and Day 14 in CTL (from 78.2% +/- 0.7% to 81.9% +/- 0.7%), but not in COC, animals (from 76.7% +/- 0.8% to 78.9% +/- 0.8% at Day 7 and from 76.8% +/- 1.1% to 79.3% +/- 0.8% at Day 14). Epinephrine induced a significant increase in contractile response in CTL, but not in COC, rats at Day 7 and had no effect on fractional area of change at 14 days of age in either CTL or COC animals. Our results indicate that perinatal cocaine exposure does not modify resting contractile function but attenuates the contractile response to beta-adrenoceptor stimulation in the neonatal rat. These results suggest that perinatal cocaine exposure may lead to decreased responsiveness to inotropic drugs during the early neonatal period.

Adrenergic alpha-Agonists↗