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

The hemodynamic manifestations of right ventricular dysfunction after ischemic injury depend not only on the severity of injury but also on the degree of coexistent left ventricular dysfunction. A better understanding of right ventricular failure and of optimal therapies has been hindered in part by lack of suitable experimental models of selective and differential ventricular injury. Therefore, we developed a technique of differential ventricular myocardial protection during a period of global cardiac ischemia and examined the effect of such an injury on intrinsic right and left ventricular myocardial function, metabolism, and regional blood flow. Twenty-six dogs were subjected to 30 minutes of ischemia while being supported by cardiopulmonary bypass. During ischemia, right and left ventricular myocardial temperatures were independently varied by selective ventricular endomyocardial thermal regulation. Nine dogs underwent right and left ventricular normothermic ischemia, eight underwent right and left ventricular hypothermic ischemia, and nine underwent right ventricular normothermic and left ventricular hypothermic ischemia. In both ventricles, normothermic ischemia resulted in greater depression of ventricular ability to generate stroke work as a function of end-diastolic dimension (p less than 0.05), greater depletion of myocardial adenine nucleotide content (p less than 0.05), and greater subendocardial reperfusion hyperemia (p less than 0.05). Myocardial temperature of the contralateral ventricle during ischemia had no effect (p = not significant) on intrinsic ventricular functional, metabolic, or regional blood flow response to injury. For a given degree of right ventricular injury assessed by these parameters, the degree of left ventricular injury could be independently varied by as much as 50%. This is a particularly suitable model for the investigation of acute right ventricular failure.
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PMID:Differential ventricular ischemic injury: an experimental model of right ventricular failure with a variable degree of left ventricular dysfunction. 317 5

Postoperative low cardiac output is the most common cause of death in patients undergoing elective repair of tetralogy of Fallot. The incidence is much higher than in elective adult bypass operations for coronary artery disease. To explain this difference, we investigated 16 children having elective repair of tetralogy (mean age 6.3 years). Myocardial biopsy specimens obtained during bypass before arrest, at the end of cold arrest by blood cardioplegia, and after 30 minutes of reperfusion were studied for adenosine triphosphate and lactate levels. Myocardium was submitted for microscopic study shortly after the onset of ischemia. The operation was successful in reducing right ventricular-pulmonary artery gradients from 82 +/- 28 to 9 +/- 1 mm Hg, yet seven patients required significant inotropic support (dopamine, greater than 5 micrograms/kg/min) for more than 24 hours and 12 patients needed prolonged use of digoxin and diuretics for right ventricular failure. Tissue levels of adenosine triphosphate and lactate in the tetralogy groups were compared with those in 20 adults with coronary artery disease having similar myocardial protection techniques. Adenosine triphosphate levels in the tetralogy group decreased during cross-clamping (41 +/- 8 minutes) from 24 +/- 3 to 16 +/- 2 mmol/kg dry weight (mean +/- 1 standard error), with a marked further drop after reperfusion to 9 +/- 2 mmol/kg (p less than 0.01). Adenosine triphosphate levels in the group with coronary disease also decreased from 20 +/- 1 to 16 +/- 1 mmol/kg after a longer cross-clamp time (70 +/- 17 minutes) but remained at 15 +/- 2 mmol/kg after reperfusion. Tissue lactate levels in the tetralogy group rose markedly during ischemia and remained elevated after reperfusion. In contrast, lactate levels in the group with coronary disease rose moderately during ischemia and returned to normal early on reperfusion. Microscopic study revealed focal myocyte necrosis in tetralogy of Fallot. Our findings, which demonstrate inadequate myocardial protection of patients with tetralogy during repair, with depression of adenosine triphosphate and increased lactate during ischemia and reperfusion, suggest a defect in oxidative metabolism. The drop in adenosine triphosphate after reperfusion in the patients with tetralogy implicates reperfusion injury as a mechanism of myocardial damage.
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PMID:Inadequate myocardial protection with cold cardioplegic arrest during repair of tetralogy of Fallot. 325 36

To determine the evolutionary changes in right and left ventricular function in acute myocardial infarction, 3 serial gated blood pool scans were performed in 76 patients within 24 hours (24 H), at 10 days (10 D) and 3 months (3 M) following the onset of myocardial infarction. The patients were divided into 3 groups: ANT (anterior MI), INF (inferior MI without right ventricular dysfunction) and RVF (inferior MI with right ventricular dysfunction). LVEF in ANT was significantly lower than that of INF and RVF at 24 H, 10 D and 3 M. The ratio of right ventricular volume to LV volume (RVV/LVV) was compared among 3 groups. The mean values of RVV/LVV in RVF were 1.3 through 24 H and 3 M and they were significantly higher than the other two groups. The RVV/LVV in ANT and INF were around 1.0. LVEDVI in RVF was rather smaller than that of ANT and INF. LVESVI in ANT at 24 H was significantly larger than that of INF and RVF and the mean value of LVESVI in ANT were around 60 ml/M2 from 24 H to 3 M. LVEF in ANT, RVF and INF did not increase significantly during peak exercise at 3 M. However, quantitative regional wall motion analysis revealed that regional wall motion of R2 (posterolateral wall motion) in ANT and R5 (septal wall motion) in INF decreased significantly during peak exercise. These impairments in regional wall motion might be due to the exacerbation of ischemia of non-infarcted area.
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PMID:Evolutionary changes in left and right ventricular function in acute myocardial infarction. 327 98

This investigation examined the efficacy of right atrial-pulmonary artery bypass (RA-PA) during acute ischemia of the right ventricle. The right coronary artery (RCA) was ligated in 25 open chest, open pericardium sheep. Control animals (n = 15) were resuscitated with only intravenous fluids. In the experimental animals (n = 10) RA-PA bypass was initiated 5 minutes after right coronary occlusion. Sixty percent (9/15) of the control animals died within 90 minutes of RCA occlusion from refractory ventricular arrhythmia or right ventricular failure. Four of 10 RA-PA animals died within 2 hours of RCA occlusion from severe pulmonary hemorrhage and arterial oxygen desaturation when high flow rates (2.5 to 3.5 L/min) were initially instituted. In these animals, lung histologic findings demonstrated extensive hemorrhage into the alveolar spaces. After 6 hours of RCA occlusion in the six surviving control animals, there were significant increases in central venous pressure and right ventricular end-diastolic cord length (relative ventricular volume change measured by ultrasonic crystal analysis), and a significant decrease in the cardiac output. In contrast, during RCA occlusion in the six surviving animals on RA-PA bypass, cardiac output was well maintained, and there was a significant decrease in central venous pressure and end-diastolic length. The percent of change from baseline in end-diastolic length correlated inversely with the percent of change from baseline in cardiac output (r = -0.81, p less than 0.01). By crystal violet and triphenyltetrazolium chloride dye techniques, the mean percentage area of necrosis to area of risk was significantly less for the RA-PA group compared with the control group (5.6% versus 67.1%, p less than 0.0001). In this experimental model, RA-PA bypass effectively unloaded the acutely ischemic right ventricle, maintained systemic cardiac output, and significantly reduced right ventricular infarction size. Further investigations with this ventricular support modality are needed to determine its effects on pulmonary pathophysiology.
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PMID:Efficacy of right ventricular unloading during right coronary artery occlusion in an experimental model. 373 46

The hypothesis of this study was that inadequate right ventricular hypothermia contributes to the right ventricular dysfunction occasionally observed after cardiac operations. Dogs were placed on cardiopulmonary bypass, and 60 minute periods of hypothermic myocardial ischemia were imposed. Left ventricular temperature was always maintained at 15 degrees C and right ventricular temperatures were maintained at 15 degrees C (Group I, n = 8), 25 degrees C (Group II, n = 8), and 35 degrees C (Group III, n = 8). These temperatures were produced by infusion of hypothermic crystalloid cardioplegic solution and appropriate topical cooling and heating of the left and right ventricles, respectively. Multiple indices of ventricular function were obtained 15, 30, 45, and 60 minutes after bypass and compared to prebypass control values. In all Group I animals (left ventricular temperature = 15 degrees C, right ventricular temperature = 15 degrees C), postischemic indices of right ventricular function were not different from control values (p = NS). In Group II (left ventricular temperature = 15 degrees C, right ventricular temperature = 25 degrees C), two animals died 30 and 45 minutes after bypass, respectively, of right ventricular failure. In the other six animals in Group II, all indices of right ventricular function were significantly reduced (p less than 0.05) except for right ventricular systolic pressure. In Group III (left ventricular temperature = 15 degrees C, right ventricular temperature = 35 degrees C), two animals could not be weaned from cardiopulmonary bypass because of right ventricular akinesia. Six animals were weaned from bypass, but two died 15 minutes, one died 30 minutes, and one 45 minutes after bypass. Two animals lived 60 minutes, but all indices of right ventricular function were decreased. Failure to maintain right ventricular temperatures below 25 degrees C during 1 hour of cardiac ischemia in the dog can result in fatal right ventricular failure.
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PMID:Acute right ventricular failure is caused by inadequate right ventricular hypothermia. 397 74

High-energy phosphate metabolites of the canine heart were analyzed before coronary artery occlusion and after 15 minutes of ischemia, and the results were then correlated with the occurrence of ventricular fibrillation upon reperfusion (RVF). Animals which developed VF upon reperfusion after 15 minutes of ischemia had lower levels of creatine phosphate and endocardial adenosine triphosphate (ATP), and increased accumulation of the catabolites of ATP metabolism, inosine and hypoxanthine. Animals which developed RVF also had lower levels of regional myocardial blood flow in the center of the ischemic zone during the period of coronary occlusion. Occluded bed size was the same in dogs which did and did not develop RVF. These data suggest that VF upon reflow is associated with more severe ischemia and an increase in high-energy phosphate catabolism during the period of ischemia.
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PMID:Alterations in the distribution of high-energy phosphates during ischemia in a canine model of reperfusion-induced ventricular fibrillation. 403 84

Between January 1968 and March 1980, 202 hearts had been transplanted into 185 patients at Stanford University Medical Center. Occasionally, patients after transplantation develop myocardial failure which is amenable only to retransplantation. Sixteen patients underwent initial orthotopic allograft using standard techniques. Eight patients developed accelerated arteriosclerotic coronary disease, six had unrelenting rejection, and two had donor heart dysrrhythmia or right ventricular failure requiring retransplantation. One patient required a third transplant because of donor left ventricular ischemia. All sequential transplants were managed similarly to the primary transplant. Of the initial transplant hearts at risk, 60% survived for more than 1 year, and 57% survived for more than 2 years. These results are similar to those of patients not requiring retransplantation. Of the secondary transplant hearts at risk, 31% survived for more than 1 year and 29% survived for more than 2 years. The severity of infection and/or rejection contributed most significantly to secondary heart transplant mortality. Sequential orthotopic cardiac transplantation offers an acceptable alternative to patients with allograft failure. Survival is not as favorable as with initial transplantation because of the prolonged immunosuppression during sequential transplantation.
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PMID:Sequential orthotopic heart transplantation in man. 700 86

Right ventricular failure during acute pressure overload has been attributed to ischemia which occurs when maximal coronary vasodilation is achieved so that further increases in myocardial blood flow cannot occur. To test the hypothesis that coronary vasodilator reserve is exhausted during acute right ventricular pressure overload, right and left ventricular myocardial blood flow was measured in 14 awake dogs during progressive pulmonary artery occlusion; coronary vasodilator reserve was tested by infusion of adenosine (4 microM/kg per min) before and during pulmonary artery occlusion. Right ventricular myocardial blood flow rose from 0.77 +/- 0.09 ml/min per g (mean +/- SEM) during control conditions to 1.69 +/- 0.27 ml/min per g during moderate pulmonary artery occlusion (P less than 0.01). With further pulmonary artery occlusion to cause increased right ventricular end-diastolic pressure and decreased aortic pressure, a selective decrease in myocardial blood flow to the right ventricular subendocardium was observed, and the right ventricular subendocardial-to-subepicardial blood flow ratio fell from 1.36 +/- 0.14 to 0.77 +/- 0.06 (P less than 0.05). With restoration of mean aortic pressure to control levels, right ventricular systolic pressure increased, right ventricular end-diastolic pressure decreased, and the right ventricular subendocardial-to-subepicardial ratio increased to 1.36 +/- 0.18 (P less than 0.01). Adenosine infusion during pulmonary artery occlusion in five dogs caused an increase in mean right ventricular blood flow (1.11 +/- 0.10 to 2.25 +/- 0.30; P less than 0.05). This increase was most marked in the outer layers but, nevertheless, was also significant in the subendocardium. These data indicate that acute severe right ventricular pressure overload may be associated with right ventricular subendocardial hypoperfusion, even when coronary vasodilator reserve is not exhausted.
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PMID:Transmural right ventricular blood flow during acute pulmonary artery hypertension in the sedated dog. Evidence for subendocardial ischemia despite residual vasodilator reserve. 709 29

To evaluate the possibility of inadequate right ventricular protection during operation, the temperatures of the anterior myocardium of the right ventricle and the middle of the interventricular septum were compared at ten-minute intervals throughout the period of continuous coronary ischemia in 130 consecutive patients. Systemic temperature was lowered to 23 degrees C, using cardiopulmonary bypass. Cardiac arrest was induced by aortic cross-clamping and infusion of cold cardioplegic solution. Cold solution was reinfused as necessary to maintain septal temperatures at less than 20 degrees C. Despite the use of superior and inferior vena caval cannulation for control of venous return, it was more difficult to maintain the right ventricle at the desired degree of myocardial hypothermia than the left ventricle. The difference between left and right ventricular temperatures was as great as 19 degrees C. In 80% of the observations (n = 1,010), the right ventricle was warmer than the left ventricle. The most frequently occurring temperature differences (left ventricle minus right ventricle) were in the 2 degrees to 3 degrees C range. These data indicate that it is more difficult to maintain hypothermia in the right ventricle. Concern for the left ventricle alone may be misleading. An alarming degree of rewarming may occur in the right ventricle and thereby contribute to right ventricular dysfunction and unilateral right ventricular failure.
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PMID:Asymmetrical myocardial hypothermia during hypothermic cardioplegia. 711 50

Acute PE may lead to right ventricular dilatation and failure. Through ventricular interdependence and decreased left ventricular filling, cardiac output and systemic circulation also may be compromised. The associated decrease in coronary perfusion pressure to the acutely overloaded right ventricle may produce ischemia and worsening right heart failure. This downward cycle of right ventricular failure and ischemia may ultimately progress to right ventricular infarction, circulatory arrest, and death. Certain clinical findings, hemodynamic values, and, particularly, echocardiographic signs can identify right ventricular dysfunction after PE. Detection of right ventricular hypokinesis helps to stratify patients' risk, because right ventricular dysfunction confers a worse prognosis than does normal right ventricular function after PE. The concept of "hemodynamic instability" after PE should be expanded to include right ventricular dilatation and wall motion abnormalities, even among normotensive patients. Aggressive intervention with thrombolytic therapy, vasoactive agents, or mechanical embolectomy may improve right ventricular function and clinical outcome.
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PMID:Right ventricular dysfunction after acute pulmonary embolism: pathophysiologic factors, detection, and therapeutic implications. 748 82


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