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At least 1,549 records · Page 86Linked to original sources
PubMed1994

An amrinone bolus prior to weaning from cardiopulmonary bypass improves cardiac function in mitral valve surgery patients.

This double-blind, randomized study was performed to assess the effectiveness of a single bolus dose of 2 mg/kg of amrinone given during cardiopulmonary bypass (CPB) to patients undergoing mitral valve surgery. Outcome variables were hemodynamic function and the number and amount of vasopressors or inotropes required to wean from CPB. In amrinone-treated patients, cardiac index (CI) increased significantly by 48 +/- 14% following CPB (T3) versus 10 +/- 10% for placebo-treated patients (P = 0.029). Similarly, on arrival in the intensive care unit (T4), CI was increased by 52 +/- 20% in amrinone patients versus 8 +/- 8% for placebo patients (P = 0.04). There was a corresponding decrease in systemic vascular resistance index of 47 +/- 6% at T3 in the amrinone patients versus 10 +/- 14% in placebo patients (P = 0.001), and a decrease of 30 +/- 7% at T4 versus an increase of 10 +/- 22% for the placebo patients (P = 0.036). There was no difference in other measured hemodynamic variables. While on CPB, mean arterial pressure at 5 minutes following administration of the study drug was decreased in amrinone patients by 20 +/- 4% versus 4 +/- 3% in placebo patients (P = 0.005), but was no different at 10 and 15 minutes. There were no statistically significant differences in the number of patients who required supplemental inotropes or vasopressors either during CPB, following separation from CPB, or upon arrival in the ICU. Thus, amrinone improved CI without changing pulmonary vascular resistance or the requirement for supplemental inotropes or vasopressors in patients undergoing elective mitral valve surgery.

Aged↗
PubMed1988

Functional cardiac assessment before and after left ventricular anterior aneurysm repair, especially as related to work capacity.

Clinical, angiographic and hemodynamic parameters were assessed preoperatively and 12-20 weeks (mean +/- SD: 14 +/- 2) after left ventricular anterior aneurysmectomy in 31 consecutive patients. In 18 patients, associated coronary artery bypass surgery was necessary (1.4 grafts/patient). One patient with mitral valve insufficiency postoperatively required mitral valve replacement. No other complications and no deaths arose. The working capacity of the patients, as measured by bicycle exercise testing, compared a stage of exercise that the patient reached to the expected level of exercise for a normal person of the same sex, age and body surface. Expressed as percent of normals it increased from 39.3 +/- 28.9% (mean +/- SD) to 60.8 +/- 15.5% (p less than 0.001), angina-pectoris-free working capacity increased from 52.6 +/- 41.4 to 89.2 +/- 33.2 W (p less than 0.001). Left ventricular end-diastolic volume was determined by simultaneous biplane angiography and decreased from 277.1 +/- 84.7 to 191.0 +/- 49.1 ml (p less than 0.001). Ejection fraction increased from 35.4 +/- 12.4 to 41.0 +/- 9.6% (p less than 0.05). Left ventricular end-diastolic pressure after angiography decreased from 24.6 +/- 9.2 to 21.1 +/- 11.3 mm Hg (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1983

Cardiac function and peripheral circulatory adjustments in patients with acute myocardial infarction. Observations during the early stage of AMI.

Since little is known concerning the effect of different types of cardiac dysfunction on the peripheral circulation in acute myocardial infarction, cardiac and peripheral circulatory hemodynamics were measured simultaneously and sequentially in the Coronary Care Unit in 40 patients with acute myocardial infarction (AMI) using a Swan-Ganz catheter and venous occlusion plethysmography. Patients were classified by clinical assessment (Killip) and into four hemodynamic subsets (HS) according to pulmonary capillary wedge pressure (PCWP) and cardiac index (CI) measures obtained by invasive central hemodynamic monitoring (Forrester): uncomplicated AMI, HS-I (PCWP less than or equal to 18 mmHg, CI greater than 2.2 L/min/m2) 15; pulmonary congestion, HS-II (PCWP greater than 18 mmHg, CI greater than 2.2 L/min/m2) 15; peripheral hypoperfusion, HS-III (PCWP less than or equal to 18 mmHg, CI less than or equal to 2.2 L/min/m2) 4; cardiogenic shock, HS-IV (PCWP greater than 18 mmHg, CI less than or equal to 2.2 L/min/m2) 6. Measurements taken within 48 hours after the onset of AMI showed significantly lower calf blood flow (p less than 0.05) and calf venous capacitance (p less than 0.01) and higher calf vascular resistance (p less than 0.05) in all AMI classifications compared to 10 normal subjects. In uncomplicated AMI group (Killip I and HS-I) calf blood flow and venous capacitance were significantly reduced while calf vascular resistance remained unchanged from normal. In AMI complicated by pulmonary congestion (Killip II and HS-II), in addition to reduced calf venous capacitance, calf blood flow was further significantly reduced (p less than 0.05) due, in part, to a rise in calf vascular resistance (p less than 0.05). In AMI complicated by severe heart failure and shock (Killip III, VI and HS-IV), mean changes in the periphery were not statistically different from those seen in patients with pulmonary congestion alone. In patients with AMI complicated by poor peripheral perfusion (HS-III), the peripheral changes did not show significant differences from those seen in uncomplicated AMI (HS-I). Significant correlations were found between calf blood flow and PCWP (r = -0.37, p less than 0.05) and CVP (r = -0.31, p less than 0.05); calf vascular resistance and PCWP (r = +0.36, p less than 0.05) and systemic vascular resistance (r = +0.43, p less than 0.01). Sequential daily peripheral hemodynamic changes in 14 H-I patients not requiring specific therapy showed that calf blood flow took 5 days, calf vascular resistance 3 days and calf venous capacitance 7 days to return to within normal levels.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1975

Cardiac function early after repair of tetralogy of Fallot.

Hemodynamics of 12 patients with tetralogy of Fallot were monitored during the first 72 hours after surgical repair. Total immediate repair in 5 patients was followed after 24 hours by a greater decrease in cardiac index than that observed in the group of 4 patients with previous palliative shunt (minus 25 plus or minus 6 vs. minus 1 plus or minus 7 per cent, p smaller than 0.025). This difference disappeared after 48 hours, and the short-term follow-up periods of these two groups were equally smooth. Six patients with pulmonary stenosis requiring the placement of an outflow patch had higher right ventricular filling pressures (after 24 hours 13.8 vs. 10.8 mm. Hg, p smaller than 0.025; 2 to 4 weeks later 9.6 vs. 5.5 mm. Hg, p smaller than 0.05), suggestive of a persistent right ventricular depression. This ventricular depression must be attributed to the induced pulmonary insufficiency and to the presence of akinetic areas. Both these factors should therefore be carefully minimized during the surgical procedure.

Adolescent↗
PubMed1982

Cardiac function in Duchenne's muscular dystrophy. Results of 10-year follow-up study and noninvasive tests.

The purposes of this study were to: (1) evaluate the progression of cardiac involvement in Duchenne's muscular dystrophy using systolic time intervals (PEP/LVET); (2) determine if the degree of cardiac involvement bears a relation to the severity of skeletal muscle disease; and (3) describe the M-mode and two-dimensional echocardiographic findings. In 1970, systolic time intervals were studied in 16 patients. During the 10-year interim, two patients were lost to follow-up study, and five patients died. Nine remaining patients were re-studied in 1980 with M-mode and two-dimensional echocardiography as well as systolic time intervals. The PEP/LVET value of these nine patients increased from 0.37 +/- 0.05 (mean +/- SD) in 1970 to 0.47 +/- 0.07 (p less than 0.005) in 1980. Three patients remained ambulatory, and their PEP/LVET value (0.41 +/- 0.04) was significantly better than that of the nonambulatory patients (0.50 +/- 0.07, p less than 0.05). The M-mode echocardiography percentage diameter change was also worse in the nonambulatory group (21 +/- 4 percent versus 34 +/- 7 percent, p less than 0.02). The five patients who were nonambulatory in 1970 died in the intervening 10 years. This study demonstrated that the heart disease of Duchenne's muscular dystrophy is progressive and that the severity of skeletal muscle disease is probably associated with the degree of cardiac dysfunction.

Adolescent↗
PubMed2005

Effects of rHu-EPO on myocyte apoptosis and cardiac function following acute myocardial infarction in rats.

SUMMARY: The mechanisms of rHu-EPO attenuating the apoptosis after myocardial infarction in rats were studied. Thirty-two rats were divided into three groups: sham operation group (Sham), acute myocardial infarction group (MI) and rHu-EPO-treated group (MI+ EPO). Acute myocardial infarction model was made by ligating the anterior descending coronary artery. rHu-EPO was administered i. p. in MI+EPO group at the dose of 5 000 IU/kg body weight immediately after the ligation. Each rat in MI+EPO group received the same dose of rHu-EPO daily the next 6 days. On the 14th day all rats underwent hemodynamic measurements and then killed. The samples were examined with HE stain, immunohistochemistry technique (bcl-2, bax) and TUNEL dyeing. The results showed that hemodynamic function in MI+ EPO group was much better than in MI group. The number of the cells positive for bax and TUNEL in MI+ EPO group was less than that in MI group. The number of the cells positive for bcl-2 in MI+ EPO group was more than that in MI group. These findings suggested that rHu-EPO could treat myocardial infarction by preventing apoptosis and attenuating post-infarction deterioration in hemodynamic function.

Animals↗
PubMed1984

Potassium deficiency and cardiac function: experimental and clinical aspects.

Intra- and extracellular potassium and magnesium gradients in cellular membranes are essential factors of physiologic functions. Intestinal and renal loss of these ions cause predominantly a decrease in cellular potassium and magnesium by lowering the extra-cellular concentrations. In close connection with these changes, the permeability of cellular membranes for ions and, consequently, the excitability of skeletal and heart muscle cells are altered. Changes in the excitation, i.e. increased rising rate of the action potential and alterations of the refractory period, provoke cardiac arrhythmias. It is assumed that in contrast to chronic potassium deficiency the net changes which are caused by a reduction of extracellular potassium in acute deficiency states predispose to glycoside toxicity. These changes may therefore explain the clinical observation that acute hypokalemia is associated with a greater glycoside sensitivity than chronic potassium deficiency. Recent findings indicate that antikaliuretic substances can prevent the incidence of cardiac arrhythmias and may reduce glycoside sensitivity of the heart not only by antikaliuretic effects, but also by a possible direct action on the myocardium. Positive inotropic actions have also been reported. The meachanism of these effects is not yet sufficiently clarified. With regard to the broad clinical application of antikaliuretic diuretics (aldosterone antagonists, amiloride and triamterene), we studied their effects on myocardial membrane properties. Aldosterone antagonists led to a significant concentration-dependent prolongation of action potential duration and, correspondingly, to a lengthening of the refractory period. Action potential duration showed a significant increase under the influence of amiloride. A shortening of the refractory period induced by glycoside was antagonized by triamterene. Thus, the administration of antikaliuretic diuretics seems to be useful in the therapy of congestive heart failure also with respect to their extrarenal cardiac effects. Potassium and magnesium deficiency significantly alter cellular membrane functions, especially under pathologic conditions as far as ionic permeability and active ion transport are concerned. We assume that these findings may further explain the persistence of cardiac arrhythmias and increased glycoside sensitivity due to potassium deficiency even after restoring normal extracellular potassium concentrations. Therefore prolonged potassium and magnesium) substitution should be provided in these conditions in spite of normal extracellular potassium concentration.

Animals↗
PubMed1985

Cardiac function in patients with cystic fibrosis: evaluation by two-dimensional and Doppler echocardiography.

Two-dimensional and Doppler echocardiography were performed in 17 consecutive hospitalized patients with cystic fibrosis aged 6 to 38 years (mean 21 +/- 9) and in 10 normal subjects aged 24 +/- 7 years. Left ventricular and right ventricular ejection fraction were measured by a computerized light pen system and Simpson's rule from two-dimensional echocardiographic apical four and two chamber views. Right ventricular wall thickness, inferior vena cava size and the presence of tricuspid regurgitation by Doppler recording were also assessed. National Institutes of Health (NIH) score of clinical severity ranged from 22 to 72 (mean 51 +/- 15) (100 = excellent, 0 = poor). Four patients, all with an NIH score of 40 or less, died of respiratory failure within 1 year of the echocardiographic study. There was no significant difference between patients with cystic fibrosis and normal subjects with regard to right ventricular ejection fraction (59 +/- 11 versus 61 +/- 10%), left ventricular ejection fraction (67 +/- 8 versus 70 +/- 8%) and right ventricular systolic (5 +/- 1 versus 5 +/- 0.5 mm) and diastolic (2.4 +/- 0.5 versus 2.5 +/- 0.5 mm) wall thicknesses. A dilated inferior vena cava and mild tricuspid regurgitation by Doppler recording were detected in only one patient. A poor correlation was found between right ventricular ejection fraction and NIH clinical score (r = 0.26), chest X-ray score (r = 0.29) and pulmonary function tests. It is concluded that right and left ventricular systolic function is preserved in patients with moderately severe cystic fibrosis; clinical status in these patients is probably determined by the pulmonary rather than cardiac involvement.

Adolescent↗
PubMed1997

Molecular mechanisms of angiotensin II in modulating cardiac function: intracardiac effects and signal transduction pathways.

Angiotensin II (Ang II), the effector peptide of the renin-angiotensin system (RAS), regulates volume and electrolyte homeostasis and is involved in cardiac and vascular cellular growth in humans and other species. This system, which has been conserved throughout evolution, plays an important role in cardiac and vascular pathology associated with hypertension, coronary heart disease, myocarditis and congestive heart failure. The traditional RAS is viewed as a system in which circulating Ang II is delivered to target organs and cells. However, in the past decade, a local RAS has been described in cardiac cells, providing evidence for autocrine and paracrine pathways by which biological actions of Ang II could be mediated. The critical actions of Ang II are mediated primarily through the AT1, G-protein (guanylyl nucleotide binding protein) coupled receptor. In addition to coupling to conventional G-protein signal transduction pathways, the AT1 receptor was recently shown to increase the tyrosine phosphorylation of several intracellular substrates, including the STAT (Signal Transducers and Activators of Transcription) family of novel transcription factors, in rat cardiac fibroblasts, myocytes and vascular smooth muscle cells, and AT1 receptor transfected CHO cells. It has been shown that Ang II stimulates the tyrosine phosphorylation and nuclear translocation of Stat1 (Stat 91) and Stat3 (Stat 92). Angiotensin II acting directly through the AT1 receptor, induces the formation of a complex of STAT proteins termed SIF (sis-inducing factor) which binds the DNA sequence, SIE (sis-inducing element) present in the promotor element of many genes. This provides evidence for a direct role of Ang II in mediating inflammatory and remodeling responses through the JAK-STAT pathway. Thus, it is likely that the JAK-STAT pathway has an important role in Ang II-mediated effects on gene transcription, cardiac and vascular cellular growth/development, and inflammatory responses.

Angiotensin II↗