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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Right ventricular hemodynamics were evaluated in 179 patients with coronary artery disease to determine the effects of chronic ischemia on right ventricular diastolic pressure. Abnormal right ventricular filling pressures occurred only in patients with an abnormal right ventricular systolic pressure or an abnormal left ventricular end-diastolic pressure. Of the 63 patients whose right ventricle was stressed by an increased systolic load secondary to passive pulmonary hypertension, 44 (72 percent) had an abnormal right ventricular end-diastolic pressure. In this group obstruction of vessels serving the right ventricular free wall or septum, or both, was almost universal (43 of 44, 98 percent) and a significantly increased incidence of inferior infarction (P less than 0.05) was noted. Such obstruction was significantly less frequent in patients with normal filling pressures (10 of 17, 59 percent; P less than 0.001). Compared with patients with coronary artery disease, patients with passive pulmonary hypertension due to aortic stenosis or mitral stenosis had significantly greater degrees of pulmonary hypertension (P less than 0.05) yet slightly lesser elevations of right ventricular end-diastolic pressure. These data suggest that in patients with ischemic heart disease the right ventricle exhibits diastolic dysfunction at lower levels of afterload stress than it would with normal coronary blood flow.
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PMID:Right ventricular diastolic pressure in coronary artery disease. 50 30

The left ventricular dysfunction following acute pulmowary hypertension remains unexplained. We wondered if acute pulmonary hypertension could alter the transmural flow distribution within the left ventricular myocardium, independent of coronary flow and perfusion pressure. We used a canine preparation in which the left coronary system was perfused at constant flow and induced a two- to three-fold increase in pulmonary artery pressure by banding the pulmonary artery. Regional myocardial blood flow of the left coronary system was measured using radioactive microspheres, injected into the left coronary system before and after 10-30 min of banding of the pulmonary artery. The left ventricular subendocardial:epicardial ratio fell by 12 and 31% (p less than 0.05) of control value, 10 and 30 min, respectively, after banding of the pulmonary artery, the total flow to the left coronary system being kept constant. Left atrial mean pressure increased from 2.9 +/- 2.4 to 3.6 +/- 1.9 and 6.0 +/- 2.1 (p less than 0.05) following banding. The mechanism of the redistribution of coronary flow may relate to inappropriate vasodilation of the right septal myocardium with consequent relative left ventricular subendocardial hypoperfusion which might aggravate left ventricular ischemia in the presence of hypotension and hypoxia.
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PMID:Redistribution in left ventricular regional flow following acute right ventricular pressure overload. 63 69

Use of extracorporeal circulation is mandatory in heart-lung and en bloc double-lung transplantation. However, no criteria exist to predict the necessity of its application during single-lung transplantation for parenchymal lung diseases. We therefore reviewed our experience in 23 patients undergoing single-lung transplantation for idiopathic pulmonary fibrosis. All patients were evaluated by preoperative right heart catheterization. For intraoperative monitoring, a pulmonary artery thermodilution catheter was placed in the contralateral lung to repeatedly assess pulmonary artery pressure, cardiac output, and pulmonary vascular resistance. Extracorporeal circulation was necessary during graft implantation in 4 patients, whereas 19 patients underwent operation without it. Preoperative demographic patient data, time of ischemia, and hemodynamic values obtained preoperatively and before the clamping of the pulmonary artery showed no significant differences between groups. In contrast, after the clamping of the pulmonary artery, a significant drop in cardiac index of about 1.5 L.min-1.m-2 (p less than 0.01) and a concomitant rise in pulmonary vascular resistance (p less than 0.01) was observed in the group requiring extracorporeal circulation, whereas these variables showed no significant changes in the other 19 patients. Pulmonary artery pressure rose significantly in both groups (p less than 0.05), without significant differences between them. It is concluded that intraoperative assessment of cardiac index and pulmonary vascular resistance is essential for estimation of cardiac performance during single-lung transplantation. A decrease in cardiac index of more than 1.5 L.min-1.m-2 after the clamping of the pulmonary artery rather than the degree of pulmonary hypertension is indicative of the need of extracorporeal circulation.
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PMID:Predictive criteria for the need of extracorporeal circulation in single-lung transplantation. 141 23

Bilateral lung transplantation (BLT) is a recently described procedure based on two sequential single-lung transplantations (SLT), which are performed by a transverse sternobithoracotomy. It does not require either cardiac arrest or routine use of cardiopulmonary bypass (CPB). The intraoperative management of 10 patients suffering from end-stage pulmonary disease is reported. Implantation of the first graft is quite similar to a SLT. Problems encountered during this procedure (ie, hypoxemia, hypercapnia, or low cardiac output) were due to restricted pulmonary and cardiac reserve. Preoperative and intraoperative assessment of the recipient's respiratory and cardiac status was, therefore, of prime importance. Mild preoperative pulmonary hypertension, well-preserved right ventricular function, and removal of the less well-perfused lung limited these difficulties; no patient required partial CPB at this stage. During the second lung implantation, gas exchange was provided by the first grafted lung. Measurements of pulmonary vascular resistance (PVR), venous admixture (Qva/Qt), and dead space (VD/VT) assessed with the arterial-to-end-tidal CO2 difference were used to confirm the adequacy of perfusion and V/Q matching. In one patient, partial CPB was instituted because of surgical difficulty related to inadequate size matching of the lungs. In the other patients, first graft function was satisfactory and the second graft was implanted without CPB. With chest closure, PVR returned to nearly normal values (range, 57-293, mean 167 dynes.s.cm-5) and Qva/Qt increased (range, 3 to 36, mean 20%). This limited series demonstrates that CPB is optional during this procedure. Good selection of recipients and donors, good lung preservation methods, and a short duration of cold ischemia are essential to success.
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PMID:Anesthesia for bilateral lung transplantation without cardiopulmonary bypass: initial experience and review of intraoperative problems. 149 95

Pulmonary vasodilator therapy during increased right ventricular (RV) afterload and insufficient RV myocardial perfusion might further impair RV performance by lowering systemic and, thus, coronary perfusion pressure. This hypothesis was tested by initially inducing pulmonary hypertension (80% increase in resting pulmonary artery pressure by injection of autologous muscle) and subsequent right coronary artery stenosis (40% decrease in flow by external cuff occlusion) in eight open-chest dogs. Then the effects of nitroglycerin (5 micrograms.kg-1.min-1), prostaglandin E1 (0.2 microgram.kg-1.min-1), and hydralazine (mean 0.14 mg/kg) on global and regional (ultrasonic dimension technique) RV performance and coronary hemodynamics (electromagnetic flow probes) were determined. Following all three drugs, right coronary artery flow decreased by 40-65% (mean values) accompanied by severe regional myocardial dysfunction suggestive of ischemia (akinesis, systolic lengthening, and postsystolic shortening). Heart rates increased by 20-40%; aortic pressure decreased by 15-25%; and RV end-diastolic pressure remained unchanged. Despite similarly adverse effects on regional RV performance and comparable effects on heart rate, perfusion and filling pressures with all three drugs, RV systolic pressure, RV dP/dt, and pulmonary artery pressure during nitroglycerin and prostaglandin E1 remained unchanged, and stroke volume and pulmonary artery flow decreased, but they all increased or were maintained (stroke volume) during hydralazine. Gas exchange was not affected by any of the vasodilators. Thus, in this model of combined acute pulmonary hypertension and right coronary artery insufficiency, nitroglycerin, prostaglandin E1, and hydralazine elicited severe regional dysfunction suggestive of ischemia, probably related to concomitant increases in heart rate and decreases in coronary perfusion pressure. Despite such evidence of severe regional RV ischemia, hydralazine maintained global RV pump function. These results indicate 1) that in the presence of increased RV afterload and coronary insufficiency, reduction in coronary perfusion pressure during pulmonary vasodilator therapy may be deleterious, and 2) that even severe regional myocardial ischemia may not necessarily be accompanied by respective changes in global hemodynamics and thus may go undetected.
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PMID:Myocardial ischemia during vasodilator therapy in a canine model of pulmonary hypertension and coronary insufficiency. 157 47

Nicardipine i.v. bolus (5 mg/5 min) was administered in the pulmonary artery trunk in 13 patients (2 f, 11 m), mean age 48 +/- 8 yrs, affected by ischemia congestive heart failure, with pulmonary hypertension (pulmonary vascular resistances greater than 6 U.W. and/or systolic pulmonary artery blood pressure greater than or equal to 60 mmHg). The vasodilatation induced by nicardipine caused a rapid improvement of all hemodynamic parameters, with a significant reduction of systemic and pulmonary pressures and resistances; in addition, cardiac output increased significantly. Even if heart rate decreased and mean right atrial pressure fell, their variation did not reach statistical significance. These beneficial effects are attributable to the vasodilator action of nicardipine on the systemic and pulmonary vascular districts. Therefore, in the hemodynamic evaluation of patients with ischemic cardiomyopathy proposed for heart transplantation, we propose the employment of nicardipine in testing the vascular reactivity in cases with secondary pulmonary hypertension.
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PMID:[Bolus nicardipine in the hemodynamic assessment for heart transplantation of patients with severe failure of ischemic origin and high pulmonary resistance]. 180 48

The importance of right ventricular (RV) function in maintaining global cardiac performance is the focus of this discussion. The physiological determinants of normal right ventricular function will be discussed, with particular emphasis on the afterload and contractility characteristics of the right ventricle. Numerous clinical conditions have been shown to affect RV performance. These conditions include positive-pressure ventilation, ischemia, pulmonary hypertension, and cardiac surgery. Present methods for the perioperative evaluation of RV function include angiography, radionuclide techniques, thermodilution techniques, echocardiography, and magnetic resonance imaging. Traditional modalities for the treatment of RV dysfunction consist of pharmacological interventions (i.e., vasodilators and inotropes) and/or mechanical assist devices. Newer pharmacological strategies for the treatment of RV failure and associated pulmonary hypertension include the phosphodiesterase fraction III inhibitors and the prostaglandins, specifically PGE1. In summary, the accurate evaluation of perioperative RV performance combined with new treatment options will ensure maximal preservation of RV performance.
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PMID:Right ventricular function and failure: a review. 181 51

Long-term low-flow oxygen therapy can lead to improved exercise capacity and improved hemodynamics in selected patients with pulmonary hypertension. We report a patient who presented with severe exercise limitation and anginal chest pain that appeared to result from pulmonary hypertension and predominantly right ventricular ischemia. Acute oxygen therapy led to relief of pain but no change in exercise capacity or of pulmonary hypertension. After eight months of oxygen therapy, the patient's pulmonary hypertension was unchanged, but right ventricular hypertrophy and marked increases in exercise cardiac output and exercise capacity developed. Thus, oxygen can relieve right ventricular angina and facilitate the development of compensatory hypertrophy.
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PMID:Relief of right ventricular angina and increased exercise capacity with long-term oxygen therapy. 183 Aug 39

A deformation of the left ventricular cavity is commonly observed in myocardial infarction, which directly influences the ventricular function. Even in cases without ischemia, a deformation of the left ventricle during systole or diastole is presumed to affect its function. Inward bending of the left ventricular posterobasal wall in giant left atrium is an example of the unfavourable effects of such a deformation. Systolic flattening of the left ventricle is atrial septal defect complicated by pulmonary hypertension is an example of the favourable influences by such a deformation. A regional wall motion abnormality observed in these cases is explained by the deformation attributed to the relationship between the left ventricle and left atrium or between the left and right ventricles. The relationship between the deformation and the function of the left ventricle in ventricular aneurysm can be explained well by the mode of blood turnover within the left ventricle. Contrast studies via the left atrium revealed that blood flow into the left ventricle did not reach the cardiac apex with an aneurysm, but immediately turned upwards towards the outflow tract. These results indicate that, although the left ventricle is anatomically a single cavity, it consists of functioning and non-functioning portions for blood turnover. A morphological abnormality of the left ventricle influences its function even without myocardial ischemia. It is necessary to relate all morphological changes of the left ventricle to cardiac function, regardless of the causes of a deformation.
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PMID:[Functional abnormality due to a deformation of the left ventricle: dynamic anatomy revealed using echocardiography]. 213 11

Pulmonary hypertension causes right ventricular ischemia and failure as a result of increased afterload combined with reduced coronary blood flow. Increasing coronary driving pressure by raising aortic pressure with phenylephrine has been shown to reverse right ventricular ischemia from pulmonary hypertension in animals. Since vasodilators often fail to reduce afterload, we tested whether raising the coronary driving pressure would improve right ventricular function in man. Ten patients with pulmonary hypertension had hemodynamics and right ventricular coronary driving pressure measured before and 10 minutes after a steady state was reached with a phenylephrine infusion titrated to raise aortic pressure by 25 percent. Phenylephrine caused a significant (p less than .01) increase in mean aortic pressure (84 to 108 mm Hg) and right ventricular coronary driving pressure (46 to 69 mm Hg). In response, there was a significant (p less than .01) rise in mean pulmonary artery pressure (58 to 67 mm Hg), right ventricular end-diastolic pressure (10 to 16 mm Hg) and wedge pressure (5 to 9 mm Hg), and an insignificant fall in cardiac output (3.26 to 3.09 L/min) and pulmonary artery O2 saturation (57 to 49 percent). Although phenylephrine increased right ventricular coronary driving pressure, it worsened right ventricular function as manifest by a rise in end-diastolic pressure and fall in cardiac output. Any benefit of raising right ventricular coronary driving pressure may have been offset by alpha vasoconstriction of right ventricular coronary blood flow and/or pulmonary arterial vasoconstriction. Phenylephrine does not appear to be a useful therapy of right ventricular failure from pulmonary hypertension in patients who fail vasodilators.
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PMID:The effects of phenylephrine on right ventricular performance in patients with pulmonary hypertension. 198 87


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