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 1,621 records · Page 90Linked to original sources
PubMed1982

[Cardiac functional state in arterial hypertension].

The results of studies of the function of the heart in 592 patients with hypertensive disease are reported. In 120 cases it was established that a dependence exists between the cardiac pains and the level of the diastolic arterial pressure, minute volume and the mass of the left ventricle (r = +0.822; p less than 0.01). The study of the magnitude of intramyocardial "stress" in 127 patients enabled the authors to distinguish those with "adequate" and "inadequate" hypertrophy. With submaximum exercise an inverse correlation (r = -0.78, p less than 0.01) was found to exist between the changes in the output fractions and the mass of the myocardium of the left ventricle, pointing to the latent cardiac insufficiency in patients with marked myocardial hypertrophy. Observation of 106 patients for 3-5 years has revealed hypertrophy involution in 20 out of 79 patients with the labile and in 2 out of 27 cases with a stable form of hypertension. A relationship was found to exist between the increase of the hypertrophy and the increase of the systolic arterial pressure, and between its decrease and the drop in the general peripheral resistance.

Adult↗
PubMed1983

Cardiac function monitored by impedance cardiography during changing seatback angles and anti-G suit inflation.

Impedance cardiography (IC) appears to be a promising noninvasive technique for monitoring small changes in pilot cardiovascular status during conditions simulating flight. Heart rate (HR), stroke volume (SV), cardiac output (CO), ventricular ejection time (VET), and thoracic impedance (Zo) were monitored in ten volunteers for 5 min at each of four seatback angles from vertical: 12 degrees, 30 degrees, 45 degrees, and 60 degrees. Data were also obtained at three seatback angles (12 degrees, 30 degrees, 60 degrees) for 6 min each before, during, and after inflation of the standard USAF anti-G suit to 1.5 psi. Significant differences (p less than 0.05) in HR, SV, CO, VET and Zo were observed among the four positions. Inflation of the standard anti-G suit to 1.5 psi at 1.0 +Gz did not significantly alter HR, SV, or CO; whereas, 1 min of deflation of the anti-G suit significantly altered HR, SV, CO compared to inflation values. The results suggest IC can detect small differences in HR, SV, CO, VET, and Zo within subjects as a function of minor changes in body position.

Cardiac Output↗
PubMed1990

The influence of N-acetylcysteine on cardiac function and rhythm disorders during ischemia and reperfusion.

To assess the ability of N-acetylcysteine to reduce the vulnerability of the heart to arrhythmias and improve its mechanical function during ischemia and reperfusion, groups of Langendorff-perfused rat hearts (15 per group) were subjected to 20 minutes of aerobic perfusion, 10 minutes of regional ischemia and 10 minutes of reperfusion. The hearts were perfused with N-acetylcysteine throughout the study. The incidences of ventricular premature beats and ventricular tachycardia induced by ischemia fell from 93% and 67%, in the N-acetylcysteine-free control group, to 40% and 27% with 8 microM N-acetylcysteine, to 33% and 27% with 80 microM N-acetylcysteine, and to 40% and 13% with 2000 microM N-acetylcysteine. The incidence of ventricular fibrillation induced by reperfusion was reduced from 93% to 60%, 67% and 47%, respectively. N-acetylcysteine had no significant effect upon the coronary flow and heart rate. When the ischemic period was prolonged to 30 minutes, N-acetylcysteine (8 microM) was shown to delay the time of onset of arrhythmias during ischemia and reperfusion. Thus, the incidences of ventricular premature beats and ventricular tachycardia were greatest after 15 minutes of ischemia in controls but were maximal after 18 minutes in hearts treated with N-acetylcysteine. N-acetylcysteine (8 microM) also improved the recovery of mechanical function after ischemia both in Langendorff preparations and in working preparations. In the working heart the post-ischemic recovery of aortic flow, coronary flow, cardiac output and aortic developed pressure after ischemia was improved from their control values of 30 +/- 5%, 82 +/- 2%, 43 +/- 2% and 63 +/- 4% to 59 +/- 7%, 98 +/- 5%, 71 +/- 3% and 80 +/- 6% respectively. Our results support the concept that agents which can alter redox state may exert protective effects against myocardial injury during both ischemia and reperfusion.

Acetylcysteine↗
PubMed1991

Biochemical assessment of cardiac function and damage in animal species. A review of the current approach of the academic, governmental and industrial institutions represented by the Animal Clinical Chemistry Association.

Species differences in metabolism, tissue localization, specificity and sensitivity for cardiac damage influence the choice of biochemical investigation used in the assessment of cardiotoxicity. The tests currently used in toxicological studies are broadly categorized herein as enzymes and other proteins, lipids and electrolytes; some limitations of these tests are also discussed.

Alanine Transaminase↗
PubMed1976

Pharmacological mechanisms for left ventricular unloading in clinical congestive heart failure. Differential effects of nitroprusside, phentolamine, and nitroglycerin on cardiac function and peripheral circulation.

We compared cardiocirculatory actions of the commonly employed systemic vasodilators, intravenous (iv) nitroprusside (NP), iv phentolamine (PH), and sublingual nitroglycerin (NTG), causing left ventricular (LV) unloading in 29 chronic coronary subjects with congestive failure to determine whether they produce disparate responses in LV function by different relaxing actions on systemic resistance and capacitance beds. Each drug equally lowered systemic arterial pressures to a small extent, whereas heart rate rose slightly with NTG. Cardiac catheterization showed a decline in end-diastolic pressure with NTG (19 to 8 mm Hg) which was greater (P less than 0.05) than with NP and PH (21 to 11). Cardiac index increased (P less than 0.05) during NP (2.68 to 2.93 liters/min per m2) and PH (2.60 to 3.02) but was unchanged (2.83) by NTG. Stroke work increased with PH, ejection fraction rose with NP and PH, and mean ejection rate increased with each, whereas pressure-time per minute fell and end-diastolic volume decreased with each agent. Total systemic vascular resistance declined (P less than 0.001) during NP and PH (1,475 to 1,200 dynes sec cm-5) but was unchanged (1,487) by NTG. Plethysmographically, forearm vascular resistance (FVR) decreased (P less than 0.01) with NP and PH (61.6 to 39.1 mm Hg/ml per 100 g/min) but not (52.4) by NTG. The decreases in venous tone (VT) with NTG (18.2 to 9.3 mm Hg/ml) and NP (18.5 to 9.8) were greater (P less than 0.05) than with PH (18.8 to 13.1) FVR/VT percent changes of 0.96, 1.62, and 0.53 with NP, PH, and NTG indicated balanced systemic arteriolovenous relaxation by iv NP, greater arteriolar dilation with iv PH, and predominant venous dilation by sublingual NTG. Thus, vasodilators produce disparate modifications of LV function by their differing alterations of preload and impedance, which are dependent upon relative extents of relaxation of systemic resistance and capacitance vessels characteristic of each agent as used clinically.

Adult↗
PubMed1992

Improved diastolic function with the calcium antagonist nisoldipine (coat-core) in patients post myocardial infarction: results of the DEFIANT study. Doppler Flow and Echocardiography in Functional cardiac Insufficiency: Assessment of Nisoldipine Therapy.

A multicentre, randomized, double-blind, placebo-controlled, parallel-group trial was undertaken in 135 patients to determine whether 4 weeks of treatment with long-acting nisoldipine coat-core (20 mg once a day) could alter diastolic function in patients with a recent myocardial infarction and with mild left ventricular dysfunction as indicated by a left ventricular ejection fraction < or = 50%. The primary endpoint was the change in diastolic filling parameters assessed by Doppler and two-dimensional echocardiography. The mean time of admission to the study was 20 days (range 7-35) after myocardial infarction. Mean left ventricular ejection fraction was 41%. The drug increased early diastolic peak velocity at the tips of the mitral leaflet by 0.06 m.s-1 (95% confidence intervals (CI): 0.01, 0.11). The time velocity integral was increased by 1.2 cm (95% CI: 0.16, 2.27). These findings are indicative of increased early diastolic flow across the mitral valve. An important determinant appeared to be a reduced isovolumic relaxation time (by 14.7 ms, 95% CI: -22.5, -6.9). As there was no change in heart rate, systolic and diastolic blood pressure or cardiac output, afterload reduction appeared unlikely as an explanation. Peak workload on exercise was 12 watts higher in the group on nisoldipine (95% CI: 0.8, 23.3). Thus, nisoldipine was shown to improve indices of diastolic ventricular function, as well as exercise capacity, in this group of patients. The observed effects of nisoldipine may reflect an anti-ischaemic effect or be due to improved relaxation of the myocardium.

Delayed-Action Preparations↗
PubMed1996

Validation of right and left ventricular conductance and echocardiography for cardiac function studies.

BACKGROUND: Continuous estimation of left ventricular volume from instantaneous conductance has compared favorably with "gold standards," is less labor intensive, and provides real-time data. Little information exists, however, correlating right ventricular conductance with such gold standards or examining the effects of an electrical field generated in the opposite ventricle. METHODS: In open-chested sheep, right and left ventricular conductance, two-dimensional echocardiography, and thermodilution cardiac outputs were measured at steady-state conditions. After these measurements, postmortem pressure-volume relations, ventricular mass, and ventricular casting were performed. RESULTS: The corrected end-diastolic volume measured by conductance correlated well with volumes measured by echocardiography (r = 0.89), postmortem pressure-volume relations (r = 0.84), and casts (r = 0.85). Left ventricular end-diastolic volume measured by conductance did not differ significantly from other standards by analysis of variance. The presence of an electrical field in the opposite ventricle did not affect measured conductance in the studied ventricle. CONCLUSIONS: Conductance is useful for the measurement of right and left ventricular end-diastolic volumes in the beating heart and is not affected by the presence of an electrical field in the opposite ventricle. Hence, conductance is a useful tool in studies involving interventricular dependence and function.

Animals↗
PubMed2001

Echocardiographic evaluation of cardiac functions and left ventricular mass in children with malnutrition.

OBJECTIVE: This study was undertaken to assess the left ventricular mass (LV Mass) and systolic and diastolic functions of the left ventricle in children with protein energy malnutrition (PEM). METHODOLOGY: Thirty children, aged between 2 months and 2 years with PEM (four kwashiorkor, seven marasmic- kwashiorkor, 19 marasmus), and 17 healthy, age-matched children, using Doppler echocardiography were studied. RESULTS: The mean LV Mass in the patients was lower than that in the controls (14.5 +/- 5.2 vs 19.8 +/- 4.7 g, P < 0.05). However, the LV Mass/body surface area was not different in the patients with PEM and in the control group (52 +/- 9.2 vs 53.9 +/- 8.2g/m(2), P > 0.05), indicating that LV Mass was reduced in proportion to decrease in body size in malnutrition. Left ventricular septal and posterior wall thickness in PEM were also lower than that in the controls, and the most significant reduction in the LV Mass, septal and posterior wall thickness were found in the kwashiorkor group. Cardiac output was reduced in proportion to decrease in body size in the patient group (1.6 +/- 0.5 vs 2.1 +/- 0.8 L/min, P < 0.05), therefore cardiac index was not significantly different between the patients and the control subjects (5.9 +/- 1.4 vs 5.7 +/- 1.6 L/min/m(2), P > 0.05). Systolic function indices including ejection fraction, fractional shortening, and diastolic function indices were not significantly different in the groups. CONCLUSIONS: We demonstrated that LV Mass and cardiac output were reduced in proportion to decrease in body size in patients with PEM, and LV systolic and diastolic functions were preserved in atrophic hearts.

Blood Pressure↗
PubMed2006

Cardiac troponin T at 96 hours after acute myocardial infarction correlates with infarct size and cardiac function.

OBJECTIVES: In clinical practice, myocardial infarct size can be estimated non-invasively by nuclear imaging techniques or contrast-enhanced magnetic resonance imaging (CE-MRI). Due to limited availability and high costs, serologic tests are frequently used as an alternative. BACKGROUND: We examined the ability of a single value of cardiac troponin T (cTnT) 96 h after onset of ST-/non-ST-segment elevation myocardial infarction (STEMI/NSTEMI) to estimate absolute infarct mass. METHODS: Functional and CE-MRI were conducted on a 1.5-T whole-body system 4 days after STEMI/NSTEMI using gadolinium (0.2 mmol/kg/bw). Infarct sizes were measured employing a specified software (Philips Medical Systems, Best, the Netherlands) and correlated with TnT measurements 96 h after onset of STEMI/NSTEMI. RESULTS: We enrolled 23 STEMI and 21 NSTEMI patients. Median time delay from onset of symptoms to balloon angioplasty was 6.25 and 9.9 h for STEMI/NSTEMI patients, respectively. Contrast-enhanced magnetic resonance imaging (median 4 days) revealed an absolute mean infarct size of 16.2 g (7.7 to 30.1 g) with a mean ejection fraction of 58% (53% to 63%) and mean stroke volume of 84 ml (75 to 107 ml). Absolute infarct sizes and median cTnT values were larger in STEMI than in NSTEMI (29.3 g [interquartile range (IQR) 16.0 to 53.0] and 1.88 microg/l [IQR 0.7 to 2.57] vs. 8.8 g [IQR 3.3 to 16.4] and 0.83 microg/l [IQR 0.4 to 1.3], both p < 0.02). Linear regression analysis was excellent for STEMI (r = 0.910) and moderate albeit still significant for NSTEMI (r = 0.575). CONCLUSIONS: A single 96-h cTnT value provides an accurate estimate of absolute infarct mass in myocardial infarction. The ability to quantify and the potential to distinguish effects of novel drug regimens on infarct size make cTnT attractive for routine practice and as a clinical end point.

Aged↗
PubMed1990

Effects of left ventricular assist for cardiogenic shock on cardiac function and organ blood flow distribution.

Organ blood flow distribution was studied in dogs subjected to a left ventricular assist device (LVAD). In normal hearts (group 1), left ventricular work was reduced by 25% when 35% of cardiac output was performed by the LVAD. Organ perfusion, measured with tracer microspheres, remained normal or slightly increased. After induction of cardiogenic shock (group 2), perfusion deteriorated in all organs, but first in the brain, kidney, and intestinum. All animals died within 1 hour. When maximal inotropic support was administered after shock (group 3), hemodynamics improved but perfusion to most organs decreased progressively and 83% of animals died within 2 hours. When the LVAD was inserted after shock but without inotropic support (group 4), perfusion of all organs became normal during LVAD except for kidney flow, which remained severely depressed (56% of preshock value). After LVAD insertion, hemodynamics did not recover completely, and 33% of the animals died within 3 hours. When use of the LVAD was combined with 5 micrograms.kg-1.min-1 of dopamine after shock (group 5), organ blood flow distribution became normal during and after LVAD use except for renal flow, which was significantly impaired (83% of preshock value). Hemodynamics recovered after LVAD use, and all animals survived in this group. We conclude that use of the LVAD combined with low-dose positive inotropic support can prevent deterioration of organ perfusion after cardiogenic shock except for kidney.

Animals↗